---
_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
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'
...