---
_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
license: https://creativecommons.org/licenses/by/4.0/
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
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title: Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron
activation in recurrent inhibitory microcircuits of rat hippocampus
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...