---
_id: '1350'
abstract:
- lang: eng
text: "The hippocampal CA3 region plays a key role in learning and memory. Recurrent
CA3–CA3\r\nsynapses are thought to be the subcellular substrate of pattern completion.
However, the\r\nsynaptic mechanisms of this network computation remain enigmatic.
To investigate these mechanisms, we combined functional connectivity analysis
with network modeling.\r\nSimultaneous recording fromup to eight CA3 pyramidal
neurons revealed that connectivity was sparse, spatially uniform, and highly enriched
in disynaptic motifs (reciprocal, convergence,divergence, and chain motifs). Unitary
connections were composed of one or two synaptic contacts, suggesting efficient
use of postsynaptic space. Real-size modeling indicated that CA3 networks with
sparse connectivity, disynaptic motifs, and single-contact connections robustly
generated pattern completion.Thus, macro- and microconnectivity contribute to
efficient\r\nmemory storage and retrieval in hippocampal networks."
acknowledged_ssus:
- _id: ScienComp
author:
- first_name: José
full_name: Guzmán, José
id: 30CC5506-F248-11E8-B48F-1D18A9856A87
last_name: Guzmán
- first_name: Alois
full_name: Schlögl, Alois
id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
last_name: Schlögl
orcid: 0000-0002-5621-8100
- first_name: Michael
full_name: Frotscher, Michael
last_name: Frotscher
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Guzmán J, Schlögl A, Frotscher M, Jonas PM. Synaptic mechanisms of pattern
completion in the hippocampal CA3 network. Science. 2016;353(6304):1117-1123.
doi:10.1126/science.aaf1836
apa: Guzmán, J., Schlögl, A., Frotscher, M., & Jonas, P. M. (2016). Synaptic
mechanisms of pattern completion in the hippocampal CA3 network. Science.
American Association for the Advancement of Science. https://doi.org/10.1126/science.aaf1836
chicago: Guzmán, José, Alois Schlögl, Michael Frotscher, and Peter M Jonas. “Synaptic
Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” Science.
American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aaf1836.
ieee: J. Guzmán, A. Schlögl, M. Frotscher, and P. M. Jonas, “Synaptic mechanisms
of pattern completion in the hippocampal CA3 network,” Science, vol. 353,
no. 6304. American Association for the Advancement of Science, pp. 1117–1123,
2016.
ista: Guzmán J, Schlögl A, Frotscher M, Jonas PM. 2016. Synaptic mechanisms of pattern
completion in the hippocampal CA3 network. Science. 353(6304), 1117–1123.
mla: Guzmán, José, et al. “Synaptic Mechanisms of Pattern Completion in the Hippocampal
CA3 Network.” Science, vol. 353, no. 6304, American Association for the
Advancement of Science, 2016, pp. 1117–23, doi:10.1126/science.aaf1836.
short: J. Guzmán, A. Schlögl, M. Frotscher, P.M. Jonas, Science 353 (2016) 1117–1123.
date_created: 2018-12-11T11:51:31Z
date_published: 2016-09-09T00:00:00Z
date_updated: 2021-01-12T06:50:04Z
day: '09'
ddc:
- '570'
department:
- _id: ScienComp
- _id: PeJo
doi: 10.1126/science.aaf1836
ec_funded: 1
file:
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month: '09'
oa: 1
oa_version: Preprint
page: 1117 - 1123
project:
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '268548'
name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P24909-B24
name: Mechanisms of transmitter release at GABAergic synapses
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5899'
pubrep_id: '823'
quality_controlled: '1'
scopus_import: 1
status: public
title: Synaptic mechanisms of pattern completion in the hippocampal CA3 network
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 353
year: '2016'
...
---
_id: '1435'
abstract:
- lang: eng
text: ATP released from neurons and astrocytes during neuronal activity or under
pathophysiological circumstances is able to influence information flow in neuronal
circuits by activation of ionotropic P2X and metabotropic P2Y receptors and subsequent
modulation of cellular excitability, synaptic strength, and plasticity. In the
present paper we review cellular and network effects of P2Y receptors in the brain.
We show that P2Y receptors inhibit the release of neurotransmitters, modulate
voltage- and ligand-gated ion channels, and differentially influence the induction
of synaptic plasticity in the prefrontal cortex, hippocampus, and cerebellum.
The findings discussed here may explain how P2Y1 receptor activation during brain
injury, hypoxia, inflammation, schizophrenia, or Alzheimer's disease leads to
an impairment of cognitive processes. Hence, it is suggested that the blockade
of P2Y1 receptors may have therapeutic potential against cognitive disturbances
in these states.
article_number: '1207393'
author:
- first_name: José
full_name: Guzmán, José
id: 30CC5506-F248-11E8-B48F-1D18A9856A87
last_name: Guzmán
- first_name: Zoltan
full_name: Gerevich, Zoltan
last_name: Gerevich
citation:
ama: 'Guzmán J, Gerevich Z. P2Y receptors in synaptic transmission and plasticity:
Therapeutic potential in cognitive dysfunction. Neural Plasticity. 2016;2016.
doi:10.1155/2016/1207393'
apa: 'Guzmán, J., & Gerevich, Z. (2016). P2Y receptors in synaptic transmission
and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity.
Hindawi Publishing Corporation. https://doi.org/10.1155/2016/1207393'
chicago: 'Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission
and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” Neural Plasticity.
Hindawi Publishing Corporation, 2016. https://doi.org/10.1155/2016/1207393.'
ieee: 'J. Guzmán and Z. Gerevich, “P2Y receptors in synaptic transmission and plasticity:
Therapeutic potential in cognitive dysfunction,” Neural Plasticity, vol.
2016. Hindawi Publishing Corporation, 2016.'
ista: 'Guzmán J, Gerevich Z. 2016. P2Y receptors in synaptic transmission and plasticity:
Therapeutic potential in cognitive dysfunction. Neural Plasticity. 2016, 1207393.'
mla: 'Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission
and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” Neural Plasticity,
vol. 2016, 1207393, Hindawi Publishing Corporation, 2016, doi:10.1155/2016/1207393.'
short: J. Guzmán, Z. Gerevich, Neural Plasticity 2016 (2016).
date_created: 2018-12-11T11:52:00Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2021-01-12T06:50:43Z
day: '01'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1155/2016/1207393
file:
- access_level: open_access
checksum: 8dc5c2f3d44d4775a6e7e3edb0d7a0da
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creator: system
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intvolume: ' 2016'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: Neural Plasticity
publication_status: published
publisher: Hindawi Publishing Corporation
publist_id: '5762'
pubrep_id: '580'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'P2Y receptors in synaptic transmission and plasticity: Therapeutic potential
in cognitive dysfunction'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 2016
year: '2016'
...
---
_id: '12903'
article_processing_charge: No
author:
- first_name: Alois
full_name: Schlögl, Alois
id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
last_name: Schlögl
orcid: 0000-0002-5621-8100
- first_name: Stephan
full_name: Stadlbauer, Stephan
id: 4D0BC184-F248-11E8-B48F-1D18A9856A87
last_name: Stadlbauer
citation:
ama: 'Schlögl A, Stadlbauer S. High performance computing at IST Austria: Modelling
the human hippocampus. In: AHPC16 - Austrian HPC Meeting 2016. VSC - Vienna
Scientific Cluster; 2016:37.'
apa: 'Schlögl, A., & Stadlbauer, S. (2016). High performance computing at IST
Austria: Modelling the human hippocampus. In AHPC16 - Austrian HPC Meeting
2016 (p. 37). Grundlsee, Austria: VSC - Vienna Scientific Cluster.'
chicago: 'Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at
IST Austria: Modelling the Human Hippocampus.” In AHPC16 - Austrian HPC Meeting
2016, 37. VSC - Vienna Scientific Cluster, 2016.'
ieee: 'A. Schlögl and S. Stadlbauer, “High performance computing at IST Austria:
Modelling the human hippocampus,” in AHPC16 - Austrian HPC Meeting 2016,
Grundlsee, Austria, 2016, p. 37.'
ista: 'Schlögl A, Stadlbauer S. 2016. High performance computing at IST Austria:
Modelling the human hippocampus. AHPC16 - Austrian HPC Meeting 2016. AHPC: Austrian
HPC Meeting, 37.'
mla: 'Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST
Austria: Modelling the Human Hippocampus.” AHPC16 - Austrian HPC Meeting 2016,
VSC - Vienna Scientific Cluster, 2016, p. 37.'
short: A. Schlögl, S. Stadlbauer, in:, AHPC16 - Austrian HPC Meeting 2016, VSC -
Vienna Scientific Cluster, 2016, p. 37.
conference:
end_date: 2016-02-24
location: Grundlsee, Austria
name: 'AHPC: Austrian HPC Meeting'
start_date: 2016-02-22
date_created: 2023-05-05T12:54:47Z
date_published: 2016-02-24T00:00:00Z
date_updated: 2023-05-16T07:15:14Z
day: '24'
ddc:
- '000'
department:
- _id: ScienComp
- _id: PeJo
file:
- access_level: open_access
checksum: 4a7b00362e81358d568f5e216fa03c3e
content_type: application/pdf
creator: dernst
date_created: 2023-05-16T07:03:56Z
date_updated: 2023-05-16T07:03:56Z
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file_date_updated: 2023-05-16T07:03:56Z
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language:
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url: https://vsc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc16/BOOKLET_AHPC16.pdf
month: '02'
oa: 1
oa_version: Published Version
page: '37'
publication: AHPC16 - Austrian HPC Meeting 2016
publication_status: published
publisher: VSC - Vienna Scientific Cluster
quality_controlled: '1'
status: public
title: 'High performance computing at IST Austria: Modelling the human hippocampus'
type: conference_abstract
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2016'
...
---
_id: '1432'
abstract:
- lang: eng
text: CA3–CA3 recurrent excitatory synapses are thought to play a key role in memory
storage and pattern completion. Whether the plasticity properties of these synapses
are consistent with their proposed network functions remains unclear. Here, we
examine the properties of spike timing-dependent plasticity (STDP) at CA3–CA3
synapses. Low-frequency pairing of excitatory postsynaptic potentials (EPSPs)
and action potentials (APs) induces long-term potentiation (LTP), independent
of temporal order. The STDP curve is symmetric and broad (half-width ~150 ms).
Consistent with these STDP induction properties, AP–EPSP sequences lead to supralinear
summation of spine [Ca2+] transients. Furthermore, afterdepolarizations (ADPs)
following APs efficiently propagate into dendrites of CA3 pyramidal neurons, and
EPSPs summate with dendritic ADPs. In autoassociative network models, storage
and recall are more robust with symmetric than with asymmetric STDP rules. Thus,
a specialized STDP induction rule allows reliable storage and recall of information
in the hippocampal CA3 network.
acknowledgement: 'We thank Jozsef Csicsvari and Nelson Spruston for critically reading
the manuscript. We also thank A. Schlögl for programming, F. Marr for technical
assistance and E. Kramberger for manuscript editing. '
article_number: '11552'
author:
- first_name: Rajiv Kumar
full_name: Mishra, Rajiv Kumar
id: 46CB58F2-F248-11E8-B48F-1D18A9856A87
last_name: Mishra
- first_name: Sooyun
full_name: Kim, Sooyun
id: 394AB1C8-F248-11E8-B48F-1D18A9856A87
last_name: Kim
- first_name: José
full_name: Guzmán, José
id: 30CC5506-F248-11E8-B48F-1D18A9856A87
last_name: Guzmán
orcid: 0000-0003-2209-5242
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Mishra RK, Kim S, Guzmán J, Jonas PM. Symmetric spike timing-dependent plasticity
at CA3–CA3 synapses optimizes storage and recall in autoassociative networks.
Nature Communications. 2016;7. doi:10.1038/ncomms11552
apa: Mishra, R. K., Kim, S., Guzmán, J., & Jonas, P. M. (2016). Symmetric spike
timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in
autoassociative networks. Nature Communications. Nature Publishing Group.
https://doi.org/10.1038/ncomms11552
chicago: Mishra, Rajiv Kumar, Sooyun Kim, José Guzmán, and Peter M Jonas. “Symmetric
Spike Timing-Dependent Plasticity at CA3–CA3 Synapses Optimizes Storage and Recall
in Autoassociative Networks.” Nature Communications. Nature Publishing
Group, 2016. https://doi.org/10.1038/ncomms11552.
ieee: R. K. Mishra, S. Kim, J. Guzmán, and P. M. Jonas, “Symmetric spike timing-dependent
plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative
networks,” Nature Communications, vol. 7. Nature Publishing Group, 2016.
ista: Mishra RK, Kim S, Guzmán J, Jonas PM. 2016. Symmetric spike timing-dependent
plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative
networks. Nature Communications. 7, 11552.
mla: Mishra, Rajiv Kumar, et al. “Symmetric Spike Timing-Dependent Plasticity at
CA3–CA3 Synapses Optimizes Storage and Recall in Autoassociative Networks.” Nature
Communications, vol. 7, 11552, Nature Publishing Group, 2016, doi:10.1038/ncomms11552.
short: R.K. Mishra, S. Kim, J. Guzmán, P.M. Jonas, Nature Communications 7 (2016).
date_created: 2018-12-11T11:51:59Z
date_published: 2016-05-13T00:00:00Z
date_updated: 2023-09-07T11:55:25Z
day: '13'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1038/ncomms11552
ec_funded: 1
file:
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checksum: 7e84d0392348c874d473b62f1042de22
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month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P24909-B24
name: Mechanisms of transmitter release at GABAergic synapses
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '268548'
name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '5766'
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quality_controlled: '1'
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record:
- id: '1396'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage
and recall in autoassociative networks
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2016'
...
---
_id: '1396'
abstract:
- lang: eng
text: CA3 pyramidal neurons are thought to pay a key role in memory storage and
pattern completion by activity-dependent synaptic plasticity between CA3-CA3 recurrent
excitatory synapses. To examine the induction rules of synaptic plasticity at
CA3-CA3 synapses, we performed whole-cell patch-clamp recordings in acute hippocampal
slices from rats (postnatal 21-24 days) at room temperature. Compound excitatory
postsynaptic potentials (ESPSs) were recorded by tract stimulation in stratum
oriens in the presence of 10 µM gabazine. High-frequency stimulation (HFS) induced
N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP). Although
LTP by HFS did not requier postsynaptic spikes, it was blocked by Na+-channel
blockers suggesting that local active processes (e.g.) dendritic spikes) may contribute
to LTP induction without requirement of a somatic action potential (AP). We next
examined the properties of spike timing-dependent plasticity (STDP) at CA3-CA3
synapses. Unexpectedly, low-frequency pairing of EPSPs and backpropagated action
potentialy (bAPs) induced LTP, independent of temporal order. The STDP curve was
symmetric and broad, with a half-width of ~150 ms. Consistent with these specific
STDP induction properties, post-presynaptic sequences led to a supralinear summation
of spine [Ca2+] transients. Furthermore, in autoassociative network models, storage
and recall was substantially more robust with symmetric than with asymmetric STDP
rules. In conclusion, we found associative forms of LTP at CA3-CA3 recurrent collateral
synapses with distinct induction rules. LTP induced by HFS may be associated with
dendritic spikes. In contrast, low frequency pairing of pre- and postsynaptic
activity induced LTP only if EPSP-AP were temporally very close. Together, these
induction mechanisms of synaptiic plasticity may contribute to memory storage
in the CA3-CA3 microcircuit at different ranges of activity.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Rajiv Kumar
full_name: Mishra, Rajiv Kumar
id: 46CB58F2-F248-11E8-B48F-1D18A9856A87
last_name: Mishra
citation:
ama: Mishra RK. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus.
2016.
apa: Mishra, R. K. (2016). Synaptic plasticity rules at CA3-CA3 recurrent synapses
in hippocampus. Institute of Science and Technology Austria.
chicago: Mishra, Rajiv Kumar. “Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses
in Hippocampus.” Institute of Science and Technology Austria, 2016.
ieee: R. K. Mishra, “Synaptic plasticity rules at CA3-CA3 recurrent synapses in
hippocampus,” Institute of Science and Technology Austria, 2016.
ista: Mishra RK. 2016. Synaptic plasticity rules at CA3-CA3 recurrent synapses in
hippocampus. Institute of Science and Technology Austria.
mla: Mishra, Rajiv Kumar. Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses
in Hippocampus. Institute of Science and Technology Austria, 2016.
short: R.K. Mishra, Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus,
Institute of Science and Technology Austria, 2016.
date_created: 2018-12-11T11:51:46Z
date_published: 2016-03-01T00:00:00Z
date_updated: 2023-09-07T11:55:26Z
day: '01'
ddc:
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degree_awarded: PhD
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month: '03'
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page: '83'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '5811'
related_material:
record:
- id: '1432'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
title: Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2016'
...
---
_id: '1616'
abstract:
- lang: eng
text: The hippocampus plays a key role in learning and memory. Previous studies
suggested that the main types of principal neurons, dentate gyrus granule cells
(GCs), CA3 pyramidal neurons, and CA1 pyramidal neurons, differ in their activity
pattern, with sparse firing in GCs and more frequent firing in CA3 and CA1 pyramidal
neurons. It has been assumed but never shown that such different activity may
be caused by differential synaptic excitation. To test this hypothesis, we performed
high-resolution whole-cell patch-clamp recordings in anesthetized rats in vivo.
In contrast to previous in vitro data, both CA3 and CA1 pyramidal neurons fired
action potentials spontaneously, with a frequency of ∼3–6 Hz, whereas GCs were
silent. Furthermore, both CA3 and CA1 cells primarily fired in bursts. To determine
the underlying mechanisms, we quantitatively assessed the frequency of spontaneous
excitatory synaptic input, the passive membrane properties, and the active membrane
characteristics. Surprisingly, GCs showed comparable synaptic excitation to CA3
and CA1 cells and the highest ratio of excitation versus hyperpolarizing inhibition.
Thus, differential synaptic excitation is not responsible for differences in firing.
Moreover, the three types of hippocampal neurons markedly differed in their passive
properties. While GCs showed the most negative membrane potential, CA3 pyramidal
neurons had the highest input resistance and the slowest membrane time constant.
The three types of neurons also differed in the active membrane characteristics.
GCs showed the highest action potential threshold, but displayed the largest gain
of the input-output curves. In conclusion, our results reveal that differential
firing of the three main types of hippocampal principal neurons in vivo is not
primarily caused by differences in the characteristics of the synaptic input,
but by the distinct properties of synaptic integration and input-output transformation.
acknowledgement: "The authors thank Jose Guzman for critically reading prior versions
of the manuscript. They also thank T. Asenov for\r\nengineering mechanical devices,
A. Schlögl for efficient pro-gramming, F. Marr for technical assistance, and E. Kramberger
for manuscript editing."
article_processing_charge: No
author:
- first_name: Janina
full_name: Kowalski, Janina
id: 3F3CA136-F248-11E8-B48F-1D18A9856A87
last_name: Kowalski
- first_name: Jian
full_name: Gan, Jian
id: 3614E438-F248-11E8-B48F-1D18A9856A87
last_name: Gan
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Alejandro
full_name: Pernia-Andrade, Alejandro
id: 36963E98-F248-11E8-B48F-1D18A9856A87
last_name: Pernia-Andrade
citation:
ama: Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. Intrinsic membrane properties
determine hippocampal differential firing pattern in vivo in anesthetized rats.
Hippocampus. 2016;26(5):668-682. doi:10.1002/hipo.22550
apa: Kowalski, J., Gan, J., Jonas, P. M., & Pernia-Andrade, A. (2016). Intrinsic
membrane properties determine hippocampal differential firing pattern in vivo
in anesthetized rats. Hippocampus. Wiley. https://doi.org/10.1002/hipo.22550
chicago: Kowalski, Janina, Jian Gan, Peter M Jonas, and Alejandro Pernia-Andrade.
“Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern
in Vivo in Anesthetized Rats.” Hippocampus. Wiley, 2016. https://doi.org/10.1002/hipo.22550.
ieee: J. Kowalski, J. Gan, P. M. Jonas, and A. Pernia-Andrade, “Intrinsic membrane
properties determine hippocampal differential firing pattern in vivo in anesthetized
rats,” Hippocampus, vol. 26, no. 5. Wiley, pp. 668–682, 2016.
ista: Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. 2016. Intrinsic membrane properties
determine hippocampal differential firing pattern in vivo in anesthetized rats.
Hippocampus. 26(5), 668–682.
mla: Kowalski, Janina, et al. “Intrinsic Membrane Properties Determine Hippocampal
Differential Firing Pattern in Vivo in Anesthetized Rats.” Hippocampus,
vol. 26, no. 5, Wiley, 2016, pp. 668–82, doi:10.1002/hipo.22550.
short: J. Kowalski, J. Gan, P.M. Jonas, A. Pernia-Andrade, Hippocampus 26 (2016)
668–682.
date_created: 2018-12-11T11:53:03Z
date_published: 2016-05-01T00:00:00Z
date_updated: 2023-10-17T10:02:02Z
day: '01'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1002/hipo.22550
file:
- access_level: open_access
checksum: 284b72b12fbe15474833ed3d4549f86b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:47Z
date_updated: 2020-07-14T12:45:07Z
file_id: '5033'
file_name: IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf
file_size: 905348
relation: main_file
file_date_updated: 2020-07-14T12:45:07Z
has_accepted_license: '1'
intvolume: ' 26'
issue: '5'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '05'
oa: 1
oa_version: Published Version
page: 668 - 682
publication: Hippocampus
publication_identifier:
eissn:
- 1098-1063
issn:
- 1050-9631
publication_status: published
publisher: Wiley
publist_id: '5550'
pubrep_id: '469'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Intrinsic membrane properties determine hippocampal differential firing pattern
in vivo in anesthetized rats
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 26
year: '2016'
...
---
_id: '1535'
abstract:
- lang: eng
text: Neuronal and neuroendocrine L-type calcium channels (Cav1.2, Cav1.3) open
readily at relatively low membrane potentials and allow Ca2+ to enter the cells
near resting potentials. In this way, Cav1.2 and Cav1.3 shape the action potential
waveform, contribute to gene expression, synaptic plasticity, neuronal differentiation,
hormone secretion and pacemaker activity. In the chromaffin cells (CCs) of the
adrenal medulla, Cav1.3 is highly expressed and is shown to support most of the
pacemaking current that sustains action potential (AP) firings and part of the
catecholamine secretion. Cav1.3 forms Ca2+-nanodomains with the fast inactivating
BK channels and drives the resting SK currents. These latter set the inter-spike
interval duration between consecutive spikes during spontaneous firing and the
rate of spike adaptation during sustained depolarizations. Cav1.3 plays also a
primary role in the switch from “tonic” to “burst” firing that occurs in mouse
CCs when either the availability of voltage-gated Na channels (Nav) is reduced
or the β2 subunit featuring the fast inactivating BK channels is deleted. Here,
we discuss the functional role of these “neuronlike” firing modes in CCs and how
Cav1.3 contributes to them. The open issue is to understand how these novel firing
patterns are adapted to regulate the quantity of circulating catecholamines during
resting condition or in response to acute and chronic stress.
acknowledgement: This work was supported by the Italian MIUR (PRIN 2010/2011 project
2010JFYFY2) and the University of Torino.
article_processing_charge: No
article_type: original
author:
- first_name: David H
full_name: Vandael, David H
id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
last_name: Vandael
orcid: 0000-0001-7577-1676
- first_name: Andrea
full_name: Marcantoni, Andrea
last_name: Marcantoni
- first_name: Emilio
full_name: Carbone, Emilio
last_name: Carbone
citation:
ama: Vandael DH, Marcantoni A, Carbone E. Cav1.3 channels as key regulators of neuron-like
firings and catecholamine release in chromaffin cells. Current Molecular Pharmacology.
2015;8(2):149-161. doi:10.2174/1874467208666150507105443
apa: Vandael, D. H., Marcantoni, A., & Carbone, E. (2015). Cav1.3 channels as
key regulators of neuron-like firings and catecholamine release in chromaffin
cells. Current Molecular Pharmacology. Bentham Science Publishers. https://doi.org/10.2174/1874467208666150507105443
chicago: Vandael, David H, Andrea Marcantoni, and Emilio Carbone. “Cav1.3 Channels
as Key Regulators of Neuron-like Firings and Catecholamine Release in Chromaffin
Cells.” Current Molecular Pharmacology. Bentham Science Publishers, 2015.
https://doi.org/10.2174/1874467208666150507105443.
ieee: D. H. Vandael, A. Marcantoni, and E. Carbone, “Cav1.3 channels as key regulators
of neuron-like firings and catecholamine release in chromaffin cells,” Current
Molecular Pharmacology, vol. 8, no. 2. Bentham Science Publishers, pp. 149–161,
2015.
ista: Vandael DH, Marcantoni A, Carbone E. 2015. Cav1.3 channels as key regulators
of neuron-like firings and catecholamine release in chromaffin cells. Current
Molecular Pharmacology. 8(2), 149–161.
mla: Vandael, David H., et al. “Cav1.3 Channels as Key Regulators of Neuron-like
Firings and Catecholamine Release in Chromaffin Cells.” Current Molecular Pharmacology,
vol. 8, no. 2, Bentham Science Publishers, 2015, pp. 149–61, doi:10.2174/1874467208666150507105443.
short: D.H. Vandael, A. Marcantoni, E. Carbone, Current Molecular Pharmacology 8
(2015) 149–161.
date_created: 2018-12-11T11:52:35Z
date_published: 2015-10-01T00:00:00Z
date_updated: 2021-01-12T06:51:26Z
day: '01'
department:
- _id: PeJo
doi: 10.2174/1874467208666150507105443
external_id:
pmid:
- '25966692'
intvolume: ' 8'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384372/
month: '10'
oa: 1
oa_version: Submitted Version
page: 149 - 161
pmid: 1
publication: Current Molecular Pharmacology
publication_status: published
publisher: Bentham Science Publishers
publist_id: '5636'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cav1.3 channels as key regulators of neuron-like firings and catecholamine
release in chromaffin cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2015'
...
---
_id: '1565'
abstract:
- lang: eng
text: Leptin is an adipokine produced by the adipose tissue regulating body weight
through its appetite-suppressing effect. Besides being expressed in the hypothalamus
and hippocampus, leptin receptors (ObRs) are also present in chromaffin cells
of the adrenal medulla. In the present study, we report the effect of leptin on
mouse chromaffin cell (MCC) functionality, focusing on cell excitability and catecholamine
secretion. Acute application of leptin (1 nm) on spontaneously firing MCCs caused
a slowly developing membrane hyperpolarization followed by complete blockade of
action potential (AP) firing. This inhibitory effect at rest was abolished by
the BK channel blocker paxilline (1 μm), suggesting the involvement of BK potassium
channels. Single-channel recordings in 'perforated microvesicles' confirmed that
leptin increased BK channel open probability without altering its unitary conductance.
BK channel up-regulation was associated with the phosphoinositide 3-kinase (PI3K)
signalling cascade because the PI3K specific inhibitor wortmannin (100 nm) fully
prevented BK current increase. We also tested the effect of leptin on evoked AP
firing and Ca2+-driven exocytosis. Although leptin preserves well-adapted AP trains
of lower frequency, APs are broader and depolarization-evoked exocytosis is increased
as a result of the larger size of the ready-releasable pool and higher frequency
of vesicle release. The kinetics and quantal size of single secretory events remained
unaltered. Leptin had no effect on firing and secretion in db-/db- mice lacking
the ObR gene, confirming its specificity. In conclusion, leptin exhibits a dual
action on MCC activity. It dampens AP firing at rest but preserves AP firing and
increases catecholamine secretion during sustained stimulation, highlighting the
importance of the adipo-adrenal axis in the leptin-mediated increase of sympathetic
tone and catecholamine release.
acknowledgement: "This work was supported by the Compagnia di San Paolo Foundation
‘Neuroscience Program’ to VC and ‘Progetto di Ateneo 2011-13’ to EC.\r\nWe thank
Dr Claudio Franchino for cell preparation and for providing excellent technical
support."
author:
- first_name: Daniela
full_name: Gavello, Daniela
last_name: Gavello
- first_name: David H
full_name: Vandael, David H
id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
last_name: Vandael
orcid: 0000-0001-7577-1676
- first_name: Sara
full_name: Gosso, Sara
last_name: Gosso
- first_name: Emilio
full_name: Carbone, Emilio
last_name: Carbone
- first_name: Valentina
full_name: Carabelli, Valentina
last_name: Carabelli
citation:
ama: Gavello D, Vandael DH, Gosso S, Carbone E, Carabelli V. Dual action of leptin
on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven
BK channel up-regulation in mouse chromaffin cells. Journal of Physiology.
2015;593(22):4835-4853. doi:10.1113/JP271078
apa: Gavello, D., Vandael, D. H., Gosso, S., Carbone, E., & Carabelli, V. (2015).
Dual action of leptin on rest-firing and stimulated catecholamine release via
phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells.
Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/JP271078
chicago: Gavello, Daniela, David H Vandael, Sara Gosso, Emilio Carbone, and Valentina
Carabelli. “Dual Action of Leptin on Rest-Firing and Stimulated Catecholamine
Release via Phosphoinositide 3-Kinase-Riven BK Channel up-Regulation in Mouse
Chromaffin Cells.” Journal of Physiology. Wiley-Blackwell, 2015. https://doi.org/10.1113/JP271078.
ieee: D. Gavello, D. H. Vandael, S. Gosso, E. Carbone, and V. Carabelli, “Dual action
of leptin on rest-firing and stimulated catecholamine release via phosphoinositide
3-kinase-riven BK channel up-regulation in mouse chromaffin cells,” Journal
of Physiology, vol. 593, no. 22. Wiley-Blackwell, pp. 4835–4853, 2015.
ista: Gavello D, Vandael DH, Gosso S, Carbone E, Carabelli V. 2015. Dual action
of leptin on rest-firing and stimulated catecholamine release via phosphoinositide
3-kinase-riven BK channel up-regulation in mouse chromaffin cells. Journal of
Physiology. 593(22), 4835–4853.
mla: Gavello, Daniela, et al. “Dual Action of Leptin on Rest-Firing and Stimulated
Catecholamine Release via Phosphoinositide 3-Kinase-Riven BK Channel up-Regulation
in Mouse Chromaffin Cells.” Journal of Physiology, vol. 593, no. 22, Wiley-Blackwell,
2015, pp. 4835–53, doi:10.1113/JP271078.
short: D. Gavello, D.H. Vandael, S. Gosso, E. Carbone, V. Carabelli, Journal of
Physiology 593 (2015) 4835–4853.
date_created: 2018-12-11T11:52:45Z
date_published: 2015-11-15T00:00:00Z
date_updated: 2021-01-12T06:51:38Z
day: '15'
department:
- _id: PeJo
doi: 10.1113/JP271078
external_id:
pmid:
- '26282459'
intvolume: ' 593'
issue: '22'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650409/
month: '11'
oa: 1
oa_version: Submitted Version
page: 4835 - 4853
pmid: 1
publication: Journal of Physiology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '5606'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dual action of leptin on rest-firing and stimulated catecholamine release via
phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 593
year: '2015'
...
---
_id: '1580'
abstract:
- lang: eng
text: Synapsins (Syns) are an evolutionarily conserved family of presynaptic proteins
crucial for the fine-tuning of synaptic function. A large amount of experimental
evidences has shown that Syns are involved in the development of epileptic phenotypes
and several mutations in Syn genes have been associated with epilepsy in humans
and animal models. Syn mutations induce alterations in circuitry and neurotransmitter
release, differentially affecting excitatory and inhibitory synapses, thus causing
an excitation/inhibition imbalance in network excitability toward hyperexcitability
that may be a determinant with regard to the development of epilepsy. Another
approach to investigate epileptogenic mechanisms is to understand how silencing
Syn affects the cellular behavior of single neurons and is associated with the
hyperexcitable phenotypes observed in epilepsy. Here, we examined the functional
effects of antisense-RNA inhibition of Syn expression on individually identified
and isolated serotonergic cells of the Helix land snail. We found that Helix synapsin
silencing increases cell excitability characterized by a slightly depolarized
resting membrane potential, decreases the rheobase, reduces the threshold for
action potential (AP) firing and increases the mean and instantaneous firing rates,
with respect to control cells. The observed increase of Ca2+ and BK currents in
Syn-silenced cells seems to be related to changes in the shape of the AP waveform.
These currents sustain the faster spiking in Syn-deficient cells by increasing
the after hyperpolarization and limiting the Na+ and Ca2+ channel inactivation
during repetitive firing. This in turn speeds up the depolarization phase by reaching
the AP threshold faster. Our results provide evidence that Syn silencing increases
intrinsic cell excitability associated with increased Ca2+ and Ca2+-dependent
BK currents in the absence of excitatory or inhibitory inputs.
article_processing_charge: No
article_type: original
author:
- first_name: Oscar
full_name: Brenes, Oscar
last_name: Brenes
- first_name: David H
full_name: Vandael, David H
id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
last_name: Vandael
orcid: 0000-0001-7577-1676
- first_name: Emilio
full_name: Carbone, Emilio
last_name: Carbone
- first_name: Pier
full_name: Montarolo, Pier
last_name: Montarolo
- first_name: Mirella
full_name: Ghirardi, Mirella
last_name: Ghirardi
citation:
ama: Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. Knock-down of synapsin
alters cell excitability and action potential waveform by potentiating BK and
voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience.
2015;311:430-443. doi:10.1016/j.neuroscience.2015.10.046
apa: Brenes, O., Vandael, D. H., Carbone, E., Montarolo, P., & Ghirardi, M.
(2015). Knock-down of synapsin alters cell excitability and action potential waveform
by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons.
Neuroscience. Elsevier. https://doi.org/10.1016/j.neuroscience.2015.10.046
chicago: Brenes, Oscar, David H Vandael, Emilio Carbone, Pier Montarolo, and Mirella
Ghirardi. “Knock-down of Synapsin Alters Cell Excitability and Action Potential
Waveform by Potentiating BK and Voltage Gated Ca2 Currents in Helix Serotonergic
Neurons.” Neuroscience. Elsevier, 2015. https://doi.org/10.1016/j.neuroscience.2015.10.046.
ieee: O. Brenes, D. H. Vandael, E. Carbone, P. Montarolo, and M. Ghirardi, “Knock-down
of synapsin alters cell excitability and action potential waveform by potentiating
BK and voltage gated Ca2 currents in Helix serotonergic neurons,” Neuroscience,
vol. 311. Elsevier, pp. 430–443, 2015.
ista: Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. 2015. Knock-down
of synapsin alters cell excitability and action potential waveform by potentiating
BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience.
311, 430–443.
mla: Brenes, Oscar, et al. “Knock-down of Synapsin Alters Cell Excitability and
Action Potential Waveform by Potentiating BK and Voltage Gated Ca2 Currents in
Helix Serotonergic Neurons.” Neuroscience, vol. 311, Elsevier, 2015, pp.
430–43, doi:10.1016/j.neuroscience.2015.10.046.
short: O. Brenes, D.H. Vandael, E. Carbone, P. Montarolo, M. Ghirardi, Neuroscience
311 (2015) 430–443.
date_created: 2018-12-11T11:52:50Z
date_published: 2015-12-17T00:00:00Z
date_updated: 2021-01-12T06:51:44Z
day: '17'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1016/j.neuroscience.2015.10.046
file:
- access_level: open_access
checksum: af2c4c994718c7be417eba0dc746aac9
content_type: application/pdf
creator: dernst
date_created: 2020-05-15T06:50:20Z
date_updated: 2020-07-14T12:45:02Z
file_id: '7849'
file_name: 2015_Neuroscience_Brenes.pdf
file_size: 5563015
relation: main_file
file_date_updated: 2020-07-14T12:45:02Z
has_accepted_license: '1'
intvolume: ' 311'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Submitted Version
page: 430 - 443
publication: Neuroscience
publication_status: published
publisher: Elsevier
publist_id: '5591'
quality_controlled: '1'
scopus_import: 1
status: public
title: Knock-down of synapsin alters cell excitability and action potential waveform
by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 311
year: '2015'
...
---
_id: '1615'
abstract:
- lang: eng
text: Loss-of-function mutations in the synaptic adhesion protein Neuroligin-4 are
among the most common genetic abnormalities associated with autism spectrum disorders,
but little is known about the function of Neuroligin-4 and the consequences of
its loss. We assessed synaptic and network characteristics in Neuroligin-4 knockout
mice, focusing on the hippocampus as a model brain region with a critical role
in cognition and memory, and found that Neuroligin-4 deletion causes subtle defects
of the protein composition and function of GABAergic synapses in the hippocampal
CA3 region. Interestingly, these subtle synaptic changes are accompanied by pronounced
perturbations of γ-oscillatory network activity, which has been implicated in
cognitive function and is altered in multiple psychiatric and neurodevelopmental
disorders. Our data provide important insights into the mechanisms by which Neuroligin-4-dependent
GABAergic synapses may contribute to autism phenotypes and indicate new strategies
for therapeutic approaches.
acknowledgement: This work was supported by the Max Planck Society (N.B. and H.E.),
the European Commission (EU-AIMS FP7-115300, N.B. and H.E.; Marie Curie IRG, D.K.-B.),
the German Research Foundation (CNMPB, N.B., H.E., and F.V.), the Alexander von
Humboldt-Foundation (D.K.-B.), and the Austrian Fond zur Förderung der Wissenschaftlichen
Forschung (P 24909-B24, P.J.). M.H. was a student of the doctoral program Molecular
Physiology of the Brain. Dr. J.-M. Fritschy generously provided the GABAARγ2 antibody.
We thank F. Benseler, I. Thanhäuser, D. Schwerdtfeger, A. Ronnenberg, and D. Winkler
for valuable advice and excellent technical support. We are grateful to the staff
at the animal facility of the Max Planck Institute of Experimental Medicine for
mouse husbandry.
author:
- first_name: Matthieu
full_name: Hammer, Matthieu
last_name: Hammer
- first_name: Dilja
full_name: Krueger Burg, Dilja
last_name: Krueger Burg
- first_name: Liam
full_name: Tuffy, Liam
last_name: Tuffy
- first_name: Benjamin
full_name: Cooper, Benjamin
last_name: Cooper
- first_name: Holger
full_name: Taschenberger, Holger
last_name: Taschenberger
- first_name: Sarit
full_name: Goswami, Sarit
id: 3A578F32-F248-11E8-B48F-1D18A9856A87
last_name: Goswami
- first_name: Hannelore
full_name: Ehrenreich, Hannelore
last_name: Ehrenreich
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Frederique
full_name: Varoqueaux, Frederique
last_name: Varoqueaux
- first_name: Jeong
full_name: Rhee, Jeong
last_name: Rhee
- first_name: Nils
full_name: Brose, Nils
last_name: Brose
citation:
ama: Hammer M, Krueger Burg D, Tuffy L, et al. Perturbed hippocampal synaptic inhibition
and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports.
2015;13(3):516-523. doi:10.1016/j.celrep.2015.09.011
apa: Hammer, M., Krueger Burg, D., Tuffy, L., Cooper, B., Taschenberger, H., Goswami,
S., … Brose, N. (2015). Perturbed hippocampal synaptic inhibition and γ-oscillations
in a neuroligin-4 knockout mouse model of autism. Cell Reports. Cell Press.
https://doi.org/10.1016/j.celrep.2015.09.011
chicago: Hammer, Matthieu, Dilja Krueger Burg, Liam Tuffy, Benjamin Cooper, Holger
Taschenberger, Sarit Goswami, Hannelore Ehrenreich, et al. “Perturbed Hippocampal
Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model
of Autism.” Cell Reports. Cell Press, 2015. https://doi.org/10.1016/j.celrep.2015.09.011.
ieee: M. Hammer et al., “Perturbed hippocampal synaptic inhibition and γ-oscillations
in a neuroligin-4 knockout mouse model of autism,” Cell Reports, vol. 13,
no. 3. Cell Press, pp. 516–523, 2015.
ista: Hammer M, Krueger Burg D, Tuffy L, Cooper B, Taschenberger H, Goswami S, Ehrenreich
H, Jonas PM, Varoqueaux F, Rhee J, Brose N. 2015. Perturbed hippocampal synaptic
inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism.
Cell Reports. 13(3), 516–523.
mla: Hammer, Matthieu, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations
in a Neuroligin-4 Knockout Mouse Model of Autism.” Cell Reports, vol. 13,
no. 3, Cell Press, 2015, pp. 516–23, doi:10.1016/j.celrep.2015.09.011.
short: M. Hammer, D. Krueger Burg, L. Tuffy, B. Cooper, H. Taschenberger, S. Goswami,
H. Ehrenreich, P.M. Jonas, F. Varoqueaux, J. Rhee, N. Brose, Cell Reports 13 (2015)
516–523.
date_created: 2018-12-11T11:53:02Z
date_published: 2015-10-20T00:00:00Z
date_updated: 2021-01-12T06:52:01Z
day: '20'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1016/j.celrep.2015.09.011
file:
- access_level: open_access
checksum: 44d30fbb543774b076b4938bd36af9d7
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:23Z
date_updated: 2020-07-14T12:45:07Z
file_id: '5005'
file_name: IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf
file_size: 2314406
relation: main_file
file_date_updated: 2020-07-14T12:45:07Z
has_accepted_license: '1'
intvolume: ' 13'
issue: '3'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 516 - 523
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '5551'
pubrep_id: '470'
quality_controlled: '1'
scopus_import: 1
status: public
title: Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4
knockout mouse model of autism
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2015'
...
---
_id: '1614'
abstract:
- lang: eng
text: 'GABAergic perisoma-inhibiting fast-spiking interneurons (PIIs) effectively
control the activity of large neuron populations by their wide axonal arborizations.
It is generally assumed that the output of one PII to its target cells is strong
and rapid. Here, we show that, unexpectedly, both strength and time course of
PII-mediated perisomatic inhibition change with distance between synaptically
connected partners in the rodent hippocampus. Synaptic signals become weaker due
to lower contact numbers and decay more slowly with distance, very likely resulting
from changes in GABAA receptor subunit composition. When distance-dependent synaptic
inhibition is introduced to a rhythmically active neuronal network model, randomly
driven principal cell assemblies are strongly synchronized by the PIIs, leading
to higher precision in principal cell spike times than in a network with uniform
synaptic inhibition. '
author:
- first_name: Michael
full_name: Strüber, Michael
last_name: Strüber
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Marlene
full_name: Bartos, Marlene
last_name: Bartos
citation:
ama: Strüber M, Jonas PM, Bartos M. Strength and duration of perisomatic GABAergic
inhibition depend on distance between synaptically connected cells. PNAS.
2015;112(4):1220-1225. doi:10.1073/pnas.1412996112
apa: Strüber, M., Jonas, P. M., & Bartos, M. (2015). Strength and duration of
perisomatic GABAergic inhibition depend on distance between synaptically connected
cells. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1412996112
chicago: Strüber, Michael, Peter M Jonas, and Marlene Bartos. “Strength and Duration
of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected
Cells.” PNAS. National Academy of Sciences, 2015. https://doi.org/10.1073/pnas.1412996112.
ieee: M. Strüber, P. M. Jonas, and M. Bartos, “Strength and duration of perisomatic
GABAergic inhibition depend on distance between synaptically connected cells,”
PNAS, vol. 112, no. 4. National Academy of Sciences, pp. 1220–1225, 2015.
ista: Strüber M, Jonas PM, Bartos M. 2015. Strength and duration of perisomatic
GABAergic inhibition depend on distance between synaptically connected cells.
PNAS. 112(4), 1220–1225.
mla: Strüber, Michael, et al. “Strength and Duration of Perisomatic GABAergic Inhibition
Depend on Distance between Synaptically Connected Cells.” PNAS, vol. 112,
no. 4, National Academy of Sciences, 2015, pp. 1220–25, doi:10.1073/pnas.1412996112.
short: M. Strüber, P.M. Jonas, M. Bartos, PNAS 112 (2015) 1220–1225.
date_created: 2018-12-11T11:53:02Z
date_published: 2015-01-27T00:00:00Z
date_updated: 2021-01-12T06:52:01Z
day: '27'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1073/pnas.1412996112
ec_funded: 1
external_id:
pmid:
- '25583495'
file:
- access_level: open_access
checksum: 6703309a1f58493cf5a704211fb6ebed
content_type: application/pdf
creator: dernst
date_created: 2019-01-17T07:52:40Z
date_updated: 2020-07-14T12:45:07Z
file_id: '5838'
file_name: 2015_PNAS_Strueber.pdf
file_size: 1280860
relation: main_file
file_date_updated: 2020-07-14T12:45:07Z
has_accepted_license: '1'
intvolume: ' 112'
issue: '4'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 1220 - 1225
pmid: 1
project:
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P24909-B24
name: Mechanisms of transmitter release at GABAergic synapses
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '268548'
name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5552'
quality_controlled: '1'
scopus_import: 1
status: public
title: Strength and duration of perisomatic GABAergic inhibition depend on distance
between synaptically connected cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 112
year: '2015'
...
---
_id: '1845'
abstract:
- lang: eng
text: Based on extrapolation from excitatory synapses, it is often assumed that
depletion of the releasable pool of synaptic vesicles is the main factor underlying
depression at inhibitory synapses. In this issue of Neuron, using subcellular
patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba
(2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes
in presynaptic action potential waveform substantially contribute to synaptic
depression. Based on extrapolation from excitatory synapses, it is often assumed
that depletion of the releasable pool of synaptic vesicles is the main factor
underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular
patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba
(2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes
in presynaptic action potential waveform substantially contribute to synaptic
depression.
article_processing_charge: No
author:
- first_name: David H
full_name: Vandael, David H
id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
last_name: Vandael
orcid: 0000-0001-7577-1676
- first_name: 'Claudia '
full_name: 'Espinoza Martinez, Claudia '
id: 31FFEE2E-F248-11E8-B48F-1D18A9856A87
last_name: Espinoza Martinez
orcid: 0000-0003-4710-2082
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Vandael DH, Espinoza Martinez C, Jonas PM. Excitement about inhibitory presynaptic
terminals. Neuron. 2015;85(6):1149-1151. doi:10.1016/j.neuron.2015.03.006
apa: Vandael, D. H., Espinoza Martinez, C., & Jonas, P. M. (2015). Excitement
about inhibitory presynaptic terminals. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.03.006
chicago: Vandael, David H, Claudia Espinoza Martinez, and Peter M Jonas. “Excitement
about Inhibitory Presynaptic Terminals.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.03.006.
ieee: D. H. Vandael, C. Espinoza Martinez, and P. M. Jonas, “Excitement about inhibitory
presynaptic terminals,” Neuron, vol. 85, no. 6. Elsevier, pp. 1149–1151,
2015.
ista: Vandael DH, Espinoza Martinez C, Jonas PM. 2015. Excitement about inhibitory
presynaptic terminals. Neuron. 85(6), 1149–1151.
mla: Vandael, David H., et al. “Excitement about Inhibitory Presynaptic Terminals.”
Neuron, vol. 85, no. 6, Elsevier, 2015, pp. 1149–51, doi:10.1016/j.neuron.2015.03.006.
short: D.H. Vandael, C. Espinoza Martinez, P.M. Jonas, Neuron 85 (2015) 1149–1151.
date_created: 2018-12-11T11:54:19Z
date_published: 2015-03-18T00:00:00Z
date_updated: 2021-10-08T09:07:34Z
day: '18'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1016/j.neuron.2015.03.006
file:
- access_level: open_access
checksum: d1808550e376a0eca2a950fda017cfa6
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:07Z
date_updated: 2020-07-14T12:45:19Z
file_id: '5192'
file_name: IST-2017-822-v1+1_Perspective_Fig__Final.pdf
file_size: 411832
relation: main_file
- access_level: open_access
checksum: a279f4ae61e6c8f33d68f69a0d02097d
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:07Z
date_updated: 2020-07-14T12:45:19Z
file_id: '5193'
file_name: IST-2017-822-v1+2_Perspective_Final2.pdf
file_size: 100769
relation: main_file
file_date_updated: 2020-07-14T12:45:19Z
has_accepted_license: '1'
intvolume: ' 85'
issue: '6'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '03'
oa: 1
oa_version: Published Version
page: 1149 - 1151
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '5256'
pubrep_id: '822'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Excitement about inhibitory presynaptic terminals
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 85
year: '2015'
...
---
_id: '1834'
abstract:
- lang: eng
text: Huge body of evidences demonstrated that volatile anesthetics affect the hippocampal
neurogenesis and neurocognitive functions, and most of them showed impairment
at anesthetic dose. Here, we investigated the effect of low dose (1.8%) sevoflurane
on hippocampal neurogenesis and dentate gyrus-dependent learning. Neonatal rats
at postnatal day 4 to 6 (P4-6) were treated with 1.8% sevoflurane for 6 hours.
Neurogenesis was quantified by bromodeoxyuridine labeling and electrophysiology
recording. Four and seven weeks after treatment, the Morris water maze and contextual-fear
discrimination learning tests were performed to determine the influence on spatial
learning and pattern separation. A 6-hour treatment with 1.8% sevoflurane promoted
hippocampal neurogenesis and increased the survival of newborn cells and the proportion
of immature granular cells in the dentate gyrus of neonatal rats. Sevoflurane-treated
rats performed better during the training days of the Morris water maze test and
in contextual-fear discrimination learning test. These results suggest that a
subanesthetic dose of sevoflurane promotes hippocampal neurogenesis in neonatal
rats and facilitates their performance in dentate gyrus-dependent learning tasks.
article_processing_charge: No
article_type: original
author:
- first_name: Chong
full_name: Chen, Chong
id: 3DFD581A-F248-11E8-B48F-1D18A9856A87
last_name: Chen
- first_name: Chao
full_name: Wang, Chao
last_name: Wang
- first_name: Xuan
full_name: Zhao, Xuan
last_name: Zhao
- first_name: Tao
full_name: Zhou, Tao
last_name: Zhou
- first_name: Dao
full_name: Xu, Dao
last_name: Xu
- first_name: Zhi
full_name: Wang, Zhi
last_name: Wang
- first_name: Ying
full_name: Wang, Ying
last_name: Wang
citation:
ama: Chen C, Wang C, Zhao X, et al. Low-dose sevoflurane promoteshippocampal neurogenesis
and facilitates the development of dentate gyrus-dependent learning in neonatal
rats. ASN Neuro. 2015;7(2). doi:10.1177/1759091415575845
apa: Chen, C., Wang, C., Zhao, X., Zhou, T., Xu, D., Wang, Z., & Wang, Y. (2015).
Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development
of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. SAGE Publications.
https://doi.org/10.1177/1759091415575845
chicago: Chen, Chong, Chao Wang, Xuan Zhao, Tao Zhou, Dao Xu, Zhi Wang, and Ying
Wang. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the
Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” ASN Neuro.
SAGE Publications, 2015. https://doi.org/10.1177/1759091415575845.
ieee: C. Chen et al., “Low-dose sevoflurane promoteshippocampal neurogenesis
and facilitates the development of dentate gyrus-dependent learning in neonatal
rats,” ASN Neuro, vol. 7, no. 2. SAGE Publications, 2015.
ista: Chen C, Wang C, Zhao X, Zhou T, Xu D, Wang Z, Wang Y. 2015. Low-dose sevoflurane
promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent
learning in neonatal rats. ASN Neuro. 7(2).
mla: Chen, Chong, et al. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis
and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal
Rats.” ASN Neuro, vol. 7, no. 2, SAGE Publications, 2015, doi:10.1177/1759091415575845.
short: C. Chen, C. Wang, X. Zhao, T. Zhou, D. Xu, Z. Wang, Y. Wang, ASN Neuro 7
(2015).
date_created: 2018-12-11T11:54:16Z
date_published: 2015-04-13T00:00:00Z
date_updated: 2023-10-18T06:47:30Z
day: '13'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1177/1759091415575845
file:
- access_level: open_access
checksum: 53e16bd3fc2ae2c0d7de9164626c37aa
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:08Z
date_updated: 2020-07-14T12:45:18Z
file_id: '5057'
file_name: IST-2016-456-v1+1_ASN_Neuro-2015-Chen-.pdf
file_size: 1146814
relation: main_file
file_date_updated: 2020-07-14T12:45:18Z
has_accepted_license: '1'
intvolume: ' 7'
issue: '2'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/3.0/
month: '04'
oa: 1
oa_version: Published Version
publication: ASN Neuro
publication_status: published
publisher: SAGE Publications
publist_id: '5269'
pubrep_id: '456'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development
of dentate gyrus-dependent learning in neonatal rats
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/3.0/legalcode
name: Creative Commons Attribution 3.0 Unported (CC BY 3.0)
short: CC BY (3.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2015'
...
---
_id: '1890'
abstract:
- lang: eng
text: To search for a target in a complex environment is an everyday behavior that
ends with finding the target. When we search for two identical targets, however,
we must continue the search after finding the first target and memorize its location.
We used fixation-related potentials to investigate the neural correlates of different
stages of the search, that is, before and after finding the first target. Having
found the first target influenced subsequent distractor processing. Compared to
distractor fixations before the first target fixation, a negative shift was observed
for three subsequent distractor fixations. These results suggest that processing
a target in continued search modulates the brain's response, either transiently
by reflecting temporary working memory processes or permanently by reflecting
working memory retention.
acknowledgement: 'Funded by Austrian Science Fund (FWF) Grant Number: P 22189-B18;
European Union within the 6th Framework Programme Grant Number: 517590; State government
of Styria Grant Number: PN 4055'
author:
- first_name: Christof
full_name: Körner, Christof
last_name: Körner
- first_name: Verena
full_name: Braunstein, Verena
last_name: Braunstein
- first_name: Matthias
full_name: Stangl, Matthias
last_name: Stangl
- first_name: Alois
full_name: Schlögl, Alois
id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
last_name: Schlögl
orcid: 0000-0002-5621-8100
- first_name: Christa
full_name: Neuper, Christa
last_name: Neuper
- first_name: Anja
full_name: Ischebeck, Anja
last_name: Ischebeck
citation:
ama: 'Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. Sequential
effects in continued visual search: Using fixation-related potentials to compare
distractor processing before and after target detection. Psychophysiology.
2014;51(4):385-395. doi:10.1111/psyp.12062'
apa: 'Körner, C., Braunstein, V., Stangl, M., Schlögl, A., Neuper, C., & Ischebeck,
A. (2014). Sequential effects in continued visual search: Using fixation-related
potentials to compare distractor processing before and after target detection.
Psychophysiology. Wiley-Blackwell. https://doi.org/10.1111/psyp.12062'
chicago: 'Körner, Christof, Verena Braunstein, Matthias Stangl, Alois Schlögl, Christa
Neuper, and Anja Ischebeck. “Sequential Effects in Continued Visual Search: Using
Fixation-Related Potentials to Compare Distractor Processing before and after
Target Detection.” Psychophysiology. Wiley-Blackwell, 2014. https://doi.org/10.1111/psyp.12062.'
ieee: 'C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, and A. Ischebeck,
“Sequential effects in continued visual search: Using fixation-related potentials
to compare distractor processing before and after target detection,” Psychophysiology,
vol. 51, no. 4. Wiley-Blackwell, pp. 385–395, 2014.'
ista: 'Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. 2014.
Sequential effects in continued visual search: Using fixation-related potentials
to compare distractor processing before and after target detection. Psychophysiology.
51(4), 385–395.'
mla: 'Körner, Christof, et al. “Sequential Effects in Continued Visual Search: Using
Fixation-Related Potentials to Compare Distractor Processing before and after
Target Detection.” Psychophysiology, vol. 51, no. 4, Wiley-Blackwell, 2014,
pp. 385–95, doi:10.1111/psyp.12062.'
short: C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, A. Ischebeck,
Psychophysiology 51 (2014) 385–395.
date_created: 2018-12-11T11:54:34Z
date_published: 2014-02-11T00:00:00Z
date_updated: 2021-01-12T06:53:52Z
day: '11'
ddc:
- '000'
department:
- _id: ScienComp
- _id: PeJo
doi: 10.1111/psyp.12062
file:
- access_level: open_access
checksum: 4255b6185e774acce1d99f8e195c564d
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:44Z
date_updated: 2020-07-14T12:45:20Z
file_id: '5233'
file_name: IST-2016-442-v1+1_K-rner_et_al-2014-Psychophysiology.pdf
file_size: 543243
relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: ' 51'
issue: '4'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 385 - 395
publication: Psychophysiology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '5205'
pubrep_id: '442'
scopus_import: 1
status: public
title: 'Sequential effects in continued visual search: Using fixation-related potentials
to compare distractor processing before and after target detection'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 51
year: '2014'
...
---
_id: '2002'
abstract:
- lang: eng
text: Oriens-lacunosum moleculare (O-LM) interneurons in the CA1 region of the hippocampus
play a key role in feedback inhibition and in the control of network activity.
However, how these cells are efficiently activated in the network remains unclear.
To address this question, I performed recordings from CA1 pyramidal neuron axons,
the presynaptic fibers that provide feedback innervation of these interneurons.
Two forms of axonal action potential (AP) modulation were identified. First, repetitive
stimulation resulted in activity-dependent AP broadening. Broadening showed fast
onset, with marked changes in AP shape following a single AP. Second, tonic depolarization
in CA1 pyramidal neuron somata induced AP broadening in the axon, and depolarization-induced
broadening summated with activity-dependent broadening. Outsideout patch recordings
from CA1 pyramidal neuron axons revealed a high density of a-dendrotoxin (α-DTX)-sensitive,
inactivating K+ channels, suggesting that K+ channel inactivation mechanistically
contributes to AP broadening. To examine the functional consequences of axonal
AP modulation for synaptic transmission, I performed paired recordings between
synaptically connected CA1 pyramidal neurons and O-LM interneurons. CA1 pyramidal
neuron-O-LM interneuron excitatory postsynaptic currents (EPSCs) showed facilitation
during both repetitive stimulation and tonic depolarization of the presynaptic
neuron. Both effects were mimicked and occluded by α-DTX, suggesting that they
were mediated by K+ channel inactivation. Therefore, axonal AP modulation can
greatly facilitate the activation of O-LM interneurons. In conclusion, modulation
of AP shape in CA1 pyramidal neuron axons substantially enhances the efficacy
of principal neuron-interneuron synapses, promoting the activation of O-LM interneurons
in recurrent inhibitory microcircuits.
article_number: '0113124'
author:
- first_name: Sooyun
full_name: Kim, Sooyun
id: 394AB1C8-F248-11E8-B48F-1D18A9856A87
last_name: Kim
citation:
ama: Kim S. Action potential modulation in CA1 pyramidal neuron axons facilitates
OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus.
PLoS One. 2014;9(11). doi:10.1371/journal.pone.0113124
apa: Kim, S. (2014). Action potential modulation in CA1 pyramidal neuron axons facilitates
OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus.
PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0113124
chicago: Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons
Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of
Rat Hippocampus.” PLoS One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0113124.
ieee: S. Kim, “Action potential modulation in CA1 pyramidal neuron axons facilitates
OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus,”
PLoS One, vol. 9, no. 11. Public Library of Science, 2014.
ista: Kim S. 2014. Action potential modulation in CA1 pyramidal neuron axons facilitates
OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus.
PLoS One. 9(11), 0113124.
mla: Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates
OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus.”
PLoS One, vol. 9, no. 11, 0113124, Public Library of Science, 2014, doi:10.1371/journal.pone.0113124.
short: S. Kim, PLoS One 9 (2014).
date_created: 2018-12-11T11:55:09Z
date_published: 2014-11-19T00:00:00Z
date_updated: 2021-01-12T06:54:39Z
day: '19'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1371/journal.pone.0113124
ec_funded: 1
file:
- access_level: open_access
checksum: 85e4f4ea144f827272aaf376b2830564
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:52Z
date_updated: 2020-07-14T12:45:24Z
file_id: '5107'
file_name: IST-2016-434-v1+1_journal.pone.0113124.pdf
file_size: 5179993
relation: main_file
file_date_updated: 2020-07-14T12:45:24Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '11'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-sa/4.0/
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '268548'
name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '5074'
pubrep_id: '434'
quality_controlled: '1'
scopus_import: 1
status: public
title: Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron
activation in recurrent inhibitory microcircuits of rat hippocampus
tmp:
image: /images/cc_by_sa.png
legal_code_url: https://creativecommons.org/licenses/by-sa/4.0/legalcode
name: Creative Commons Attribution-ShareAlike 4.0 International Public License (CC
BY-SA 4.0)
short: CC BY-SA (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '2031'
abstract:
- lang: eng
text: A puzzling property of synaptic transmission, originally established at the
neuromuscular junction, is that the time course of transmitter release is independent
of the extracellular Ca2+ concentration ([Ca2+]o), whereas the rate of release
is highly [Ca2+]o-dependent. Here, we examine the time course of release at inhibitory
basket cell-Purkinje cell synapses and show that it is independent of [Ca2+]o.
Modeling of Ca2+-dependent transmitter release suggests that the invariant time
course of release critically depends on tight coupling between Ca2+ channels and
release sensors. Experiments with exogenous Ca2+ chelators reveal that channel-sensor
coupling at basket cell-Purkinje cell synapses is very tight, with a mean distance
of 10–20 nm. Thus, tight channel-sensor coupling provides a mechanistic explanation
for the apparent [Ca2+]o independence of the time course of release.
author:
- first_name: Itaru
full_name: Arai, Itaru
id: 32A73F6C-F248-11E8-B48F-1D18A9856A87
last_name: Arai
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Arai itaru, Jonas PM. Nanodomain coupling explains Ca^2+ independence of transmitter
release time course at a fast central synapse. eLife. 2014;3. doi:10.7554/eLife.04057
apa: Arai, itaru, & Jonas, P. M. (2014). Nanodomain coupling explains Ca^2+
independence of transmitter release time course at a fast central synapse. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.04057
chicago: Arai, itaru, and Peter M Jonas. “Nanodomain Coupling Explains Ca^2+ Independence
of Transmitter Release Time Course at a Fast Central Synapse.” ELife. eLife
Sciences Publications, 2014. https://doi.org/10.7554/eLife.04057.
ieee: itaru Arai and P. M. Jonas, “Nanodomain coupling explains Ca^2+ independence
of transmitter release time course at a fast central synapse,” eLife, vol.
3. eLife Sciences Publications, 2014.
ista: Arai itaru, Jonas PM. 2014. Nanodomain coupling explains Ca^2+ independence
of transmitter release time course at a fast central synapse. eLife. 3.
mla: Arai, itaru, and Peter M. Jonas. “Nanodomain Coupling Explains Ca^2+ Independence
of Transmitter Release Time Course at a Fast Central Synapse.” ELife, vol.
3, eLife Sciences Publications, 2014, doi:10.7554/eLife.04057.
short: itaru Arai, P.M. Jonas, ELife 3 (2014).
date_created: 2018-12-11T11:55:19Z
date_published: 2014-12-09T00:00:00Z
date_updated: 2021-01-12T06:54:51Z
day: '09'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.7554/eLife.04057
ec_funded: 1
file:
- access_level: open_access
checksum: c240f915450d4ebe8f95043a2a8c7b1a
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:41Z
date_updated: 2020-07-14T12:45:26Z
file_id: '5094'
file_name: IST-2016-421-v1+1_e04057.full.pdf
file_size: 2239563
relation: main_file
file_date_updated: 2020-07-14T12:45:26Z
has_accepted_license: '1'
intvolume: ' 3'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Submitted Version
project:
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P24909-B24
name: Mechanisms of transmitter release at GABAergic synapses
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '268548'
name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
publication: eLife
publication_status: published
publisher: eLife Sciences Publications
publist_id: '5041'
pubrep_id: '421'
quality_controlled: '1'
scopus_import: 1
status: public
title: Nanodomain coupling explains Ca^2+ independence of transmitter release time
course at a fast central synapse
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 3
year: '2014'
...
---
_id: '2041'
abstract:
- lang: eng
text: The hippocampus mediates several higher brain functions, such as learning,
memory, and spatial coding. The input region of the hippocampus, the dentate gyrus,
plays a critical role in these processes. Several lines of evidence suggest that
the dentate gyrus acts as a preprocessor of incoming information, preparing it
for subsequent processing in CA3. For example, the dentate gyrus converts input
from the entorhinal cortex, where cells have multiple spatial fields, into the
spatially more specific place cell activity characteristic of the CA3 region.
Furthermore, the dentate gyrus is involved in pattern separation, transforming
relatively similar input patterns into substantially different output patterns.
Finally, the dentate gyrus produces a very sparse coding scheme in which only
a very small fraction of neurons are active at any one time.
article_number: 2p
author:
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: John
full_name: Lisman, John
last_name: Lisman
citation:
ama: Jonas PM, Lisman J. Structure, function and plasticity of hippocampal dentate
gyrus microcircuits. Frontiers in Neural Circuits. 2014;8. doi:10.3389/fncir.2014.00107
apa: Jonas, P. M., & Lisman, J. (2014). Structure, function and plasticity of
hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits.
Frontiers Research Foundation. https://doi.org/10.3389/fncir.2014.00107
chicago: Jonas, Peter M, and John Lisman. “Structure, Function and Plasticity of
Hippocampal Dentate Gyrus Microcircuits.” Frontiers in Neural Circuits.
Frontiers Research Foundation, 2014. https://doi.org/10.3389/fncir.2014.00107.
ieee: P. M. Jonas and J. Lisman, “Structure, function and plasticity of hippocampal
dentate gyrus microcircuits,” Frontiers in Neural Circuits, vol. 8. Frontiers
Research Foundation, 2014.
ista: Jonas PM, Lisman J. 2014. Structure, function and plasticity of hippocampal
dentate gyrus microcircuits. Frontiers in Neural Circuits. 8, 2p.
mla: Jonas, Peter M., and John Lisman. “Structure, Function and Plasticity of Hippocampal
Dentate Gyrus Microcircuits.” Frontiers in Neural Circuits, vol. 8, 2p,
Frontiers Research Foundation, 2014, doi:10.3389/fncir.2014.00107.
short: P.M. Jonas, J. Lisman, Frontiers in Neural Circuits 8 (2014).
date_created: 2018-12-11T11:55:22Z
date_published: 2014-09-10T00:00:00Z
date_updated: 2021-01-12T06:54:55Z
day: '10'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.3389/fncir.2014.00107
file:
- access_level: open_access
checksum: 3ca57b164045523f876407e9f13a9fb8
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:38Z
date_updated: 2020-07-14T12:45:26Z
file_id: '5294'
file_name: IST-2016-424-v1+1_fncir-08-00107.pdf
file_size: 201110
relation: main_file
file_date_updated: 2020-07-14T12:45:26Z
has_accepted_license: '1'
intvolume: ' 8'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: Frontiers in Neural Circuits
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '5010'
pubrep_id: '424'
quality_controlled: '1'
scopus_import: 1
status: public
title: Structure, function and plasticity of hippocampal dentate gyrus microcircuits
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2014'
...
---
_id: '2062'
abstract:
- lang: eng
text: The success story of fast-spiking, parvalbumin-positive (PV+) GABAergic interneurons
(GABA, γ-aminobutyric acid) in the mammalian central nervous system is noteworthy.
In 1995, the properties of these interneurons were completely unknown. Twenty
years later, thanks to the massive use of subcellular patch-clamp techniques,
simultaneous multiple-cell recording, optogenetics, in vivo measurements, and
computational approaches, our knowledge about PV+ interneurons became more extensive
than for several types of pyramidal neurons. These findings have implications
beyond the “small world” of basic research on GABAergic cells. For example, the
results provide a first proof of principle that neuroscientists might be able
to close the gaps between the molecular, cellular, network, and behavioral levels,
representing one of the main challenges at the present time. Furthermore, the
results may form the basis for PV+ interneurons as therapeutic targets for brain
disease in the future. However, much needs to be learned about the basic function
of these interneurons before clinical neuroscientists will be able to use PV+
interneurons for therapeutic purposes.
article_number: '1255263'
author:
- first_name: Hua
full_name: Hu, Hua
id: 4AC0145C-F248-11E8-B48F-1D18A9856A87
last_name: Hu
- first_name: Jian
full_name: Gan, Jian
id: 3614E438-F248-11E8-B48F-1D18A9856A87
last_name: Gan
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: 'Hu H, Gan J, Jonas PM. Fast-spiking parvalbumin^+ GABAergic interneurons:
From cellular design to microcircuit function. Science. 2014;345(6196).
doi:10.1126/science.1255263'
apa: 'Hu, H., Gan, J., & Jonas, P. M. (2014). Fast-spiking parvalbumin^+ GABAergic
interneurons: From cellular design to microcircuit function. Science. American
Association for the Advancement of Science. https://doi.org/10.1126/science.1255263'
chicago: 'Hu, Hua, Jian Gan, and Peter M Jonas. “Fast-Spiking Parvalbumin^+ GABAergic
Interneurons: From Cellular Design to Microcircuit Function.” Science.
American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1255263.'
ieee: 'H. Hu, J. Gan, and P. M. Jonas, “Fast-spiking parvalbumin^+ GABAergic interneurons:
From cellular design to microcircuit function,” Science, vol. 345, no.
6196. American Association for the Advancement of Science, 2014.'
ista: 'Hu H, Gan J, Jonas PM. 2014. Fast-spiking parvalbumin^+ GABAergic interneurons:
From cellular design to microcircuit function. Science. 345(6196), 1255263.'
mla: 'Hu, Hua, et al. “Fast-Spiking Parvalbumin^+ GABAergic Interneurons: From Cellular
Design to Microcircuit Function.” Science, vol. 345, no. 6196, 1255263,
American Association for the Advancement of Science, 2014, doi:10.1126/science.1255263.'
short: H. Hu, J. Gan, P.M. Jonas, Science 345 (2014).
date_created: 2018-12-11T11:55:29Z
date_published: 2014-08-01T00:00:00Z
date_updated: 2021-01-12T06:55:03Z
day: '01'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1126/science.1255263
ec_funded: 1
file:
- access_level: open_access
checksum: a0036a589037d37e86364fa25cc0a82f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:00Z
date_updated: 2020-07-14T12:45:27Z
file_id: '5185'
file_name: IST-2017-821-v1+1_1255263JonasPVReviewTextR_Final.pdf
file_size: 215514
relation: main_file
- access_level: open_access
checksum: e1f57d2713725449cb898fdcb8ef47b8
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:01Z
date_updated: 2020-07-14T12:45:27Z
file_id: '5186'
file_name: IST-2017-821-v1+2_1255263JonasPVReviewFigures_Final.pdf
file_size: 1732723
relation: main_file
file_date_updated: 2020-07-14T12:45:27Z
has_accepted_license: '1'
intvolume: ' 345'
issue: '6196'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Submitted Version
project:
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P24909-B24
name: Mechanisms of transmitter release at GABAergic synapses
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '268548'
name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '4984'
pubrep_id: '821'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to
microcircuit function'
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 345
year: '2014'
...
---
_id: '2164'
abstract:
- lang: eng
text: 'Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe
epilepsy (TLE), has been assumed to result from a migration defect during development.
Indeed, recent studies reported that aberrant migration of neonatal-generated
dentate granule cells (GCs) increased the risk to develop epilepsy later in life.
On the contrary, in the present study, we show that fully differentiated GCs become
motile following the induction of epileptiform activity, resulting in GCD. Hippocampal
slice cultures from transgenic mice expressing green fluorescent protein in differentiated,
but not in newly generated GCs, were incubated with the glutamate receptor agonist
kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy,
we observed that KA-exposed, differentiated GCs translocated their cell bodies
and changed their dendritic organization. As found in human TLE, KA application
was associated with decreased expression of the extracellular matrix protein Reelin,
particularly in hilar interneurons. Together these findings suggest that KA-induced
motility of differentiated GCs contributes to the development of GCD and establish
slice cultures as a model to study neuronal changes induced by epileptiform activity. '
author:
- first_name: Xuejun
full_name: Chai, Xuejun
last_name: Chai
- first_name: Gert
full_name: Münzner, Gert
last_name: Münzner
- first_name: Shanting
full_name: Zhao, Shanting
last_name: Zhao
- first_name: Stefanie
full_name: Tinnes, Stefanie
last_name: Tinnes
- first_name: Janina
full_name: Kowalski, Janina
id: 3F3CA136-F248-11E8-B48F-1D18A9856A87
last_name: Kowalski
- first_name: Ute
full_name: Häussler, Ute
last_name: Häussler
- first_name: Christina
full_name: Young, Christina
last_name: Young
- first_name: Carola
full_name: Haas, Carola
last_name: Haas
- first_name: Michael
full_name: Frotscher, Michael
last_name: Frotscher
citation:
ama: Chai X, Münzner G, Zhao S, et al. Epilepsy-induced motility of differentiated
neurons. Cerebral Cortex. 2014;24(8):2130-2140. doi:10.1093/cercor/bht067
apa: Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., …
Frotscher, M. (2014). Epilepsy-induced motility of differentiated neurons. Cerebral
Cortex. Oxford University Press. https://doi.org/10.1093/cercor/bht067
chicago: Chai, Xuejun, Gert Münzner, Shanting Zhao, Stefanie Tinnes, Janina Kowalski,
Ute Häussler, Christina Young, Carola Haas, and Michael Frotscher. “Epilepsy-Induced
Motility of Differentiated Neurons.” Cerebral Cortex. Oxford University
Press, 2014. https://doi.org/10.1093/cercor/bht067.
ieee: X. Chai et al., “Epilepsy-induced motility of differentiated neurons,”
Cerebral Cortex, vol. 24, no. 8. Oxford University Press, pp. 2130–2140,
2014.
ista: Chai X, Münzner G, Zhao S, Tinnes S, Kowalski J, Häussler U, Young C, Haas
C, Frotscher M. 2014. Epilepsy-induced motility of differentiated neurons. Cerebral
Cortex. 24(8), 2130–2140.
mla: Chai, Xuejun, et al. “Epilepsy-Induced Motility of Differentiated Neurons.”
Cerebral Cortex, vol. 24, no. 8, Oxford University Press, 2014, pp. 2130–40,
doi:10.1093/cercor/bht067.
short: X. Chai, G. Münzner, S. Zhao, S. Tinnes, J. Kowalski, U. Häussler, C. Young,
C. Haas, M. Frotscher, Cerebral Cortex 24 (2014) 2130–2140.
date_created: 2018-12-11T11:56:04Z
date_published: 2014-08-01T00:00:00Z
date_updated: 2021-01-12T06:55:43Z
day: '01'
department:
- _id: PeJo
doi: 10.1093/cercor/bht067
intvolume: ' 24'
issue: '8'
language:
- iso: eng
month: '08'
oa_version: None
page: 2130 - 2140
publication: Cerebral Cortex
publication_status: published
publisher: Oxford University Press
publist_id: '4820'
quality_controlled: '1'
scopus_import: 1
status: public
title: Epilepsy-induced motility of differentiated neurons
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 24
year: '2014'
...
---
_id: '2176'
abstract:
- lang: eng
text: Electron microscopy (EM) allows for the simultaneous visualization of all
tissue components at high resolution. However, the extent to which conventional
aldehyde fixation and ethanol dehydration of the tissue alter the fine structure
of cells and organelles, thereby preventing detection of subtle structural changes
induced by an experiment, has remained an issue. Attempts have been made to rapidly
freeze tissue to preserve native ultrastructure. Shock-freezing of living tissue
under high pressure (high-pressure freezing, HPF) followed by cryosubstitution
of the tissue water avoids aldehyde fixation and dehydration in ethanol; the tissue
water is immobilized in â ̂1/450 ms, and a close-to-native fine structure of cells,
organelles and molecules is preserved. Here we describe a protocol for HPF that
is useful to monitor ultrastructural changes associated with functional changes
at synapses in the brain but can be applied to many other tissues as well. The
procedure requires a high-pressure freezer and takes a minimum of 7 d but can
be paused at several points.
author:
- first_name: Daniel
full_name: Studer, Daniel
last_name: Studer
- first_name: Shanting
full_name: Zhao, Shanting
last_name: Zhao
- first_name: Xuejun
full_name: Chai, Xuejun
last_name: Chai
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Werner
full_name: Graber, Werner
last_name: Graber
- first_name: Sigrun
full_name: Nestel, Sigrun
last_name: Nestel
- first_name: Michael
full_name: Frotscher, Michael
last_name: Frotscher
citation:
ama: Studer D, Zhao S, Chai X, et al. Capture of activity-induced ultrastructural
changes at synapses by high-pressure freezing of brain tissue. Nature Protocols.
2014;9(6):1480-1495. doi:10.1038/nprot.2014.099
apa: Studer, D., Zhao, S., Chai, X., Jonas, P. M., Graber, W., Nestel, S., &
Frotscher, M. (2014). Capture of activity-induced ultrastructural changes at synapses
by high-pressure freezing of brain tissue. Nature Protocols. Nature Publishing
Group. https://doi.org/10.1038/nprot.2014.099
chicago: Studer, Daniel, Shanting Zhao, Xuejun Chai, Peter M Jonas, Werner Graber,
Sigrun Nestel, and Michael Frotscher. “Capture of Activity-Induced Ultrastructural
Changes at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols.
Nature Publishing Group, 2014. https://doi.org/10.1038/nprot.2014.099.
ieee: D. Studer et al., “Capture of activity-induced ultrastructural changes
at synapses by high-pressure freezing of brain tissue,” Nature Protocols,
vol. 9, no. 6. Nature Publishing Group, pp. 1480–1495, 2014.
ista: Studer D, Zhao S, Chai X, Jonas PM, Graber W, Nestel S, Frotscher M. 2014.
Capture of activity-induced ultrastructural changes at synapses by high-pressure
freezing of brain tissue. Nature Protocols. 9(6), 1480–1495.
mla: Studer, Daniel, et al. “Capture of Activity-Induced Ultrastructural Changes
at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols,
vol. 9, no. 6, Nature Publishing Group, 2014, pp. 1480–95, doi:10.1038/nprot.2014.099.
short: D. Studer, S. Zhao, X. Chai, P.M. Jonas, W. Graber, S. Nestel, M. Frotscher,
Nature Protocols 9 (2014) 1480–1495.
date_created: 2018-12-11T11:56:09Z
date_published: 2014-05-29T00:00:00Z
date_updated: 2021-01-12T06:55:47Z
day: '29'
department:
- _id: PeJo
doi: 10.1038/nprot.2014.099
intvolume: ' 9'
issue: '6'
language:
- iso: eng
month: '05'
oa_version: None
page: 1480 - 1495
project:
- _id: 25BDE9A4-B435-11E9-9278-68D0E5697425
grant_number: SFB-TR3-TP10B
name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen
publication: Nature Protocols
publication_status: published
publisher: Nature Publishing Group
publist_id: '4807'
quality_controlled: '1'
scopus_import: 1
status: public
title: Capture of activity-induced ultrastructural changes at synapses by high-pressure
freezing of brain tissue
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...