---
OA_place: publisher
OA_type: hybrid
PlanS_conform: '1'
_id: '20457'
abstract:
- lang: eng
text: Patch-clamp recording of miniature postsynaptic currents (mPSCs, or ‘minis’)
is used extensively to investigate the functional properties of synapses. With
this approach, spontaneous synaptic transmission events are recorded in an attempt
to determine quantal synaptic parameters or the effect of synaptic manipulations.
However, at the majority of brain synapses these events are small, with many undetectable
due to recording noise. The effects of incomplete detection were well appreciated
in the early years of synaptic physiology analysis, but appear to be increasingly
forgotten. Here we sought to characterise the consequences of incomplete detection
on the interpretability of mini analysis, using simulated mPSC data to give full
control over event parameters. We demonstrate that commonly reported measures
such as mean event amplitude and frequency, are misrepresented by the loss of
undetected events. Probabilistic loss of small events results in detected event
amplitude distributions that appear biologically complete, yet do not reflect
the underlying synaptic properties. With both simulated and experimental datasets,
we demonstrate that specific changes in event amplitude are primarily detected
as changes in frequency, compromising classical biological interpretations. To
facilitate more robust data analysis and interpretation, we detail a means for
experimental estimation of the event detection limit and provide practical recommendations
for data analysis. Together, our study highlights how mini analysis is prone to
falsely reporting synaptic changes, raising awareness of these considerations,
and provides a framework for more robust data analysis and interpretation.
acknowledgement: This work was supported by Biological Services teams at both the
Laboratory of Molecular Biology and Ares facilities. The authors are very grateful
to Prof. Helmut Kessels and Dr. Hinze Ho for initial discussions that led to this
study, Dr. Andrew Penn for constructive feedback on the project, Xinyao Dou for
comments on the study, and Profs. Peter Jonas and Roger Nicoll for feedback on the
manuscript. Funding was provided by the Medical Research Council (MRC – MC_U105174197
to I.H.G.) and the European Union's Horizon 2020 programme through a Marie Skłodowska-Curie
Actions Individual Fellowship (MSCA-IF 101026635 to J.F.W.).
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Ingo H.
full_name: Greger, Ingo H.
last_name: Greger
- first_name: Jake
full_name: Watson, Jake
id: 63836096-4690-11EA-BD4E-32803DDC885E
last_name: Watson
orcid: 0000-0002-8698-3823
citation:
ama: Greger IH, Watson J. ‘Mini analysis’ misrepresents changes in synaptic properties
due to incomplete event detection. Journal of Physiology. 2025;603(22):7189-7205.
doi:10.1113/JP288183
apa: Greger, I. H., & Watson, J. (2025). ‘Mini analysis’ misrepresents changes
in synaptic properties due to incomplete event detection. Journal of Physiology.
Wiley. https://doi.org/10.1113/JP288183
chicago: Greger, Ingo H., and Jake Watson. “‘Mini Analysis’ Misrepresents Changes
in Synaptic Properties Due to Incomplete Event Detection.” Journal of Physiology.
Wiley, 2025. https://doi.org/10.1113/JP288183.
ieee: I. H. Greger and J. Watson, “‘Mini analysis’ misrepresents changes in synaptic
properties due to incomplete event detection,” Journal of Physiology, vol.
603, no. 22. Wiley, pp. 7189–7205, 2025.
ista: Greger IH, Watson J. 2025. ‘Mini analysis’ misrepresents changes in synaptic
properties due to incomplete event detection. Journal of Physiology. 603(22),
7189–7205.
mla: Greger, Ingo H., and Jake Watson. “‘Mini Analysis’ Misrepresents Changes in
Synaptic Properties Due to Incomplete Event Detection.” Journal of Physiology,
vol. 603, no. 22, Wiley, 2025, pp. 7189–205, doi:10.1113/JP288183.
short: I.H. Greger, J. Watson, Journal of Physiology 603 (2025) 7189–7205.
corr_author: '1'
date_created: 2025-10-12T22:01:27Z
date_published: 2025-11-15T00:00:00Z
date_updated: 2026-01-05T13:13:32Z
day: '15'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1113/JP288183
ec_funded: 1
external_id:
isi:
- '001581924700001'
pmid:
- '41015537'
file:
- access_level: open_access
checksum: 3326e49795f44a7c51c16ecbcce58cde
content_type: application/pdf
creator: dernst
date_created: 2026-01-05T13:13:06Z
date_updated: 2026-01-05T13:13:06Z
file_id: '20949'
file_name: 2025_JourPhysiology_Greger.pdf
file_size: 10875254
relation: main_file
success: 1
file_date_updated: 2026-01-05T13:13:06Z
has_accepted_license: '1'
intvolume: ' 603'
isi: 1
issue: '22'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '11'
oa: 1
oa_version: Published Version
page: 7189-7205
pmid: 1
project:
- _id: fc2be41b-9c52-11eb-aca3-faa90aa144e9
call_identifier: H2020
grant_number: '101026635'
name: Synaptic computations of the hippocampal CA3 circuitry
publication: Journal of Physiology
publication_identifier:
eissn:
- 1469-7793
issn:
- 0022-3751
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
link:
- relation: software
url: https://github.com/jakefwatson/miniplace
scopus_import: '1'
status: public
title: ‘Mini analysis’ misrepresents changes in synaptic properties due to incomplete
event 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 603
year: '2025'
...
---
_id: '6470'
abstract:
- lang: eng
text: 'Investigating neuronal activity using genetically encoded Ca2+ indicators
in behaving animals is hampered by inaccuracies in spike inference from fluorescent
tracers. Here we combine two‐photon [Ca2+] imaging with cell‐attached recordings,
followed by post hoc determination of the expression level of GCaMP6f, to explore
how it affects the amplitude, kinetics and temporal summation of somatic [Ca2+]
transients in mouse hippocampal pyramidal cells (PCs). The amplitude of unitary
[Ca2+] transients (evoked by a single action potential) negatively correlates
with GCaMP6f expression, but displays large variability even among PCs with similarly
low expression levels. The summation of fluorescence signals is frequency‐dependent,
supralinear and also shows remarkable cell‐to‐cell variability. We performed experimental
data‐based simulations and found that spike inference error rates using MLspike
depend strongly on unitary peak amplitudes and GCaMP6f expression levels. We provide
simple methods for estimating the unitary [Ca2+] transients in individual weakly
GCaMP6f‐expressing PCs, with which we achieve spike inference error rates of ∼5%. '
article_processing_charge: No
article_type: original
author:
- first_name: Tímea
full_name: Éltes, Tímea
last_name: Éltes
- first_name: Miklos
full_name: Szoboszlay, Miklos
last_name: Szoboszlay
- first_name: Margit Katalin
full_name: Szigeti, Margit Katalin
id: 44F4BDC0-F248-11E8-B48F-1D18A9856A87
last_name: Szigeti
orcid: 0000-0001-9500-8758
- first_name: Zoltan
full_name: Nusser, Zoltan
last_name: Nusser
citation:
ama: Éltes T, Szoboszlay M, Szigeti MK, Nusser Z. Improved spike inference accuracy
by estimating the peak amplitude of unitary [Ca2+] transients in weakly GCaMP6f-expressing
hippocampal pyramidal cells. Journal of Physiology. 2019;597(11):2925–2947.
doi:10.1113/JP277681
apa: Éltes, T., Szoboszlay, M., Szigeti, M. K., & Nusser, Z. (2019). Improved
spike inference accuracy by estimating the peak amplitude of unitary [Ca2+] transients
in weakly GCaMP6f-expressing hippocampal pyramidal cells. Journal of Physiology.
Wiley. https://doi.org/10.1113/JP277681
chicago: Éltes, Tímea, Miklos Szoboszlay, Margit Katalin Szigeti, and Zoltan Nusser.
“Improved Spike Inference Accuracy by Estimating the Peak Amplitude of Unitary
[Ca2+] Transients in Weakly GCaMP6f-Expressing Hippocampal Pyramidal Cells.” Journal
of Physiology. Wiley, 2019. https://doi.org/10.1113/JP277681.
ieee: T. Éltes, M. Szoboszlay, M. K. Szigeti, and Z. Nusser, “Improved spike inference
accuracy by estimating the peak amplitude of unitary [Ca2+] transients in weakly
GCaMP6f-expressing hippocampal pyramidal cells,” Journal of Physiology,
vol. 597, no. 11. Wiley, pp. 2925–2947, 2019.
ista: Éltes T, Szoboszlay M, Szigeti MK, Nusser Z. 2019. Improved spike inference
accuracy by estimating the peak amplitude of unitary [Ca2+] transients in weakly
GCaMP6f-expressing hippocampal pyramidal cells. Journal of Physiology. 597(11),
2925–2947.
mla: Éltes, Tímea, et al. “Improved Spike Inference Accuracy by Estimating the Peak
Amplitude of Unitary [Ca2+] Transients in Weakly GCaMP6f-Expressing Hippocampal
Pyramidal Cells.” Journal of Physiology, vol. 597, no. 11, Wiley, 2019,
pp. 2925–2947, doi:10.1113/JP277681.
short: T. Éltes, M. Szoboszlay, M.K. Szigeti, Z. Nusser, Journal of Physiology 597
(2019) 2925–2947.
date_created: 2019-05-19T21:59:17Z
date_published: 2019-06-01T00:00:00Z
date_updated: 2026-06-18T19:05:34Z
day: '01'
ddc:
- '570'
department:
- _id: GaNo
doi: 10.1113/JP277681
external_id:
isi:
- '000470780400013'
pmid:
- '31006863'
intvolume: ' 597'
isi: 1
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1113/JP277681
month: '06'
oa: 1
oa_version: Published Version
page: 2925–2947
pmid: 1
publication: Journal of Physiology
publication_identifier:
eissn:
- 1469-7793
issn:
- 0022-3751
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Improved spike inference accuracy by estimating the peak amplitude of unitary
[Ca2+] transients in weakly GCaMP6f-expressing hippocampal pyramidal cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 597
year: '2019'
...
---
OA_type: closed access
_id: '3822'
abstract:
- lang: eng
text: Dentate gyrus granule cells transmit action potentials (APs) along their unmyelinated
mossy fibre axons to the CA3 region. Although the initiation and propagation of
APs are fundamental steps during neural computation, little is known about the
site of AP initiation and the speed of propagation in mossy fibre axons. To address
these questions, we performed simultaneous somatic and axonal whole-cell recordings
from granule cells in acute hippocampal slices of adult mice at approximately
23 degrees C. Injection of short current pulses or synaptic stimulation evoked
axonal and somatic APs with similar amplitudes. By contrast, the time course was
significantly different, as axonal APs had a higher maximal rate of rise (464
+/- 30 V s(-1) in the axon versus 297 +/- 12 V s(-1) in the soma, mean +/- s.e.m.).
Furthermore, analysis of latencies between the axonal and somatic signals showed
that APs were initiated in the proximal axon at approximately 20-30 mum distance
from the soma, and propagated orthodromically with a velocity of 0.24 m s(-1).
Qualitatively similar results were obtained at a recording temperature of approximately
34 degrees C. Modelling of AP propagation in detailed cable models of granule
cells suggested that a approximately 4 times higher Na(+) channel density ( approximately
1000 pS mum(-2)) in the axon might account for both the higher rate of rise of
axonal APs and the robust AP initiation in the proximal mossy fibre axon. This
may be of critical importance to separate dendritic integration of thousands of
synaptic inputs from the generation and transmission of a common AP output.
article_processing_charge: No
article_type: original
author:
- first_name: Christoph
full_name: Schmidt Hieber, Christoph
last_name: Schmidt Hieber
- 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: Josef
full_name: Bischofberger, Josef
last_name: Bischofberger
citation:
ama: Schmidt Hieber C, Jonas PM, Bischofberger J. Action potential initiation and
propagation in hippocampal mossy fibre axons. The Journal of Physiology.
2008;586(7):1849-1857. doi:10.1113/jphysiol.2007.150151
apa: Schmidt Hieber, C., Jonas, P. M., & Bischofberger, J. (2008). Action potential
initiation and propagation in hippocampal mossy fibre axons. The Journal of
Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.2007.150151
chicago: Schmidt Hieber, Christoph, Peter M Jonas, and Josef Bischofberger. “Action
Potential Initiation and Propagation in Hippocampal Mossy Fibre Axons.” The
Journal of Physiology. Wiley-Blackwell, 2008. https://doi.org/10.1113/jphysiol.2007.150151 .
ieee: C. Schmidt Hieber, P. M. Jonas, and J. Bischofberger, “Action potential initiation
and propagation in hippocampal mossy fibre axons,” The Journal of Physiology,
vol. 586, no. 7. Wiley-Blackwell, pp. 1849–57, 2008.
ista: Schmidt Hieber C, Jonas PM, Bischofberger J. 2008. Action potential initiation
and propagation in hippocampal mossy fibre axons. The Journal of Physiology. 586(7),
1849–57.
mla: Schmidt Hieber, Christoph, et al. “Action Potential Initiation and Propagation
in Hippocampal Mossy Fibre Axons.” The Journal of Physiology, vol. 586,
no. 7, Wiley-Blackwell, 2008, pp. 1849–57, doi:10.1113/jphysiol.2007.150151 .
short: C. Schmidt Hieber, P.M. Jonas, J. Bischofberger, The Journal of Physiology
586 (2008) 1849–57.
date_created: 2018-12-11T12:05:21Z
date_published: 2008-03-31T00:00:00Z
date_updated: 2026-06-10T10:16:11Z
day: '31'
doi: '10.1113/jphysiol.2007.150151 '
extern: '1'
external_id:
pmid:
- '18258662'
intvolume: ' 586'
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375716/
month: '03'
oa: 1
oa_version: None
page: 1849 - 57
pmid: 1
publication: The Journal of Physiology
publication_identifier:
eissn:
- 1469-7793
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2387'
status: public
title: Action potential initiation and propagation in hippocampal mossy fibre axons
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 586
year: '2008'
...
---
OA_place: repository
OA_type: green
_id: '3825'
abstract:
- lang: eng
text: Fast-spiking parvalbumin-expressing basket cells (BCs) represent a major type
of inhibitory interneuron in the hippocampus. These cells inhibit principal cells
in a temporally precise manner and are involved in the generation of network oscillations.
Although BCs show a unique expression profile of Ca(2+)-permeable receptors, Ca(2+)-binding
proteins and Ca(2+)-dependent signalling molecules, physiological Ca(2+) signalling
in these interneurons has not been investigated. To study action potential (AP)-induced
dendritic Ca(2+) influx and buffering, we combined whole-cell patch-clamp recordings
with ratiometric Ca(2+) imaging from the proximal apical dendrites of rigorously
identified BCs in acute slices, using the high-affinity Ca(2+) indicator fura-2
or the low-affinity dye fura-FF. Single APs evoked dendritic Ca(2+) transients
with small amplitude. Bursts of APs evoked Ca(2+) transients with amplitudes that
increased linearly with AP number. Analysis of Ca(2+) transients under steady-state
conditions with different fura-2 concentrations and during loading with 200 microm
fura-2 indicated that the endogenous Ca(2+)-binding ratio was approximately 200
(kappa(S) = 202 +/- 26 for the loading experiments). The peak amplitude of the
Ca(2+) transients measured directly with 100 microm fura-FF was 39 nm AP(-1).
At approximately 23 degrees C, the decay time constant of the Ca(2+) transients
was 390 ms, corresponding to an extrusion rate of approximately 600 s(-1). At
34 degrees C, the decay time constant was 203 ms and the corresponding extrusion
rate was approximately 1100 s(-1). At both temperatures, continuous theta-burst
activity with three to five APs per theta cycle, as occurs in vivo during exploration,
led to a moderate increase in the global Ca(2+) concentration that was proportional
to AP number, whereas more intense stimulation was required to reach micromolar
Ca(2+) concentrations and to shift Ca(2+) signalling into a non-linear regime.
In conclusion, dentate gyrus BCs show a high endogenous Ca(2+)-binding ratio,
a small AP-induced dendritic Ca(2+) influx, and a relatively slow Ca(2+) extrusion.
These specific buffering properties of BCs will sharpen the time course of local
Ca(2+) signals, while prolonging the decay of global Ca(2+) signals.
article_processing_charge: No
article_type: original
author:
- first_name: Yexica
full_name: Aponte, Yexica
last_name: Aponte
- first_name: Josef
full_name: Bischofberger, Josef
last_name: Bischofberger
- 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: Aponte Y, Bischofberger J, Jonas PM. Efficient Ca(2+) buffering in fast-spiking
basket cells of rat hippocampus. The Journal of Physiology. 2008;586(8):2061-2075.
doi:10.1113/jphysiol.2007.147298
apa: Aponte, Y., Bischofberger, J., & Jonas, P. M. (2008). Efficient Ca(2+)
buffering in fast-spiking basket cells of rat hippocampus. The Journal of Physiology.
Wiley-Blackwell. https://doi.org/10.1113/jphysiol.2007.147298
chicago: Aponte, Yexica, Josef Bischofberger, and Peter M Jonas. “Efficient Ca(2+)
Buffering in Fast-Spiking Basket Cells of Rat Hippocampus.” The Journal of
Physiology. Wiley-Blackwell, 2008. https://doi.org/10.1113/jphysiol.2007.147298.
ieee: Y. Aponte, J. Bischofberger, and P. M. Jonas, “Efficient Ca(2+) buffering
in fast-spiking basket cells of rat hippocampus,” The Journal of Physiology,
vol. 586, no. 8. Wiley-Blackwell, pp. 2061–75, 2008.
ista: Aponte Y, Bischofberger J, Jonas PM. 2008. Efficient Ca(2+) buffering in fast-spiking
basket cells of rat hippocampus. The Journal of Physiology. 586(8), 2061–75.
mla: Aponte, Yexica, et al. “Efficient Ca(2+) Buffering in Fast-Spiking Basket Cells
of Rat Hippocampus.” The Journal of Physiology, vol. 586, no. 8, Wiley-Blackwell,
2008, pp. 2061–75, doi:10.1113/jphysiol.2007.147298.
short: Y. Aponte, J. Bischofberger, P.M. Jonas, The Journal of Physiology 586 (2008)
2061–75.
date_created: 2018-12-11T12:05:22Z
date_published: 2008-04-14T00:00:00Z
date_updated: 2026-05-29T11:01:59Z
day: '14'
doi: 10.1113/jphysiol.2007.147298
extern: '1'
external_id:
pmid:
- '18276734'
intvolume: ' 586'
issue: '8'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2465201/
month: '04'
oa: 1
oa_version: None
page: 2061 - 75
pmid: 1
publication: The Journal of Physiology
publication_identifier:
eissn:
- 1469-7793
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2386'
status: public
title: Efficient Ca(2+) buffering in fast-spiking basket cells of rat hippocampus
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 586
year: '2008'
...
---
OA_type: closed access
_id: '2628'
abstract:
- lang: eng
text: We aimed to estimate the number of AMPA receptors (AMPARs) bound by the quantal
transmitter packet, their single-channel conductance and their density in the
postsynaptic membrane at cerebellar Purkinje cell synapses. The synaptic and extrasynaptic
AMPARs were examined in Purkinje cells in 2- to 4-day-old rats, when they receive
synaptic inputs solely from climbing fibres (CFs). Evoked CF EPSCs and whole-cell
AMPA currents displayed roughly linear current-voltage relationships, consistent
with the presence of GluR2 subunits in synaptic and extrasynaptic AMPARs. The
mean quantal size, estimated from the miniature EPSCs (MEPSCs), was ∼300 pS. Peak-scaled
non-stationary fluctuation analysis of spontaneous EPSCs and MEPSCs gave a weighted-mean
synaptic channel conductance of ∼5 pS (∼7 pS when corrected for filtering). By
applying non-stationary fluctuation analysis to extrasynaptic currents activated
by brief glutamate pulses (5 mM), we also obtained a small single-channel conductance
estimate for extrasynaptic AMPARs (∼11 pS). This approach allowed us to obtain
a maximum open probability (Po,max) value for the extrasynaptic receptors (Po,max
= 0.72). Directly resolved extrasynaptic channel openings in the continued presence
of glutamate exhibited clear multiple-conductance levels. The mean area of the
postsynaptic density (PSD) of these synapses was 0.074 μm2, measured by reconstructing
electron-microscopic (EM) serial sections. Postembedding immunogold labelling
by anti-GluR2/3 antibody revealed that AMPARs are localised in PSDs. From these
data and by simulating error factors, we estimate that at least 66 AMPARs are
bound by a quantal transmitter packet at CF-Purkinje cell synapses, and the receptors
are packed at a minimum density of ∼900 μm-2 in the postsynaptic membrane.
article_processing_charge: No
article_type: original
author:
- first_name: Akiko
full_name: Momiyama, Akiko
last_name: Momiyama
- first_name: Rachel
full_name: Silver, Rachel
last_name: Silver
- first_name: Michael
full_name: Häusser, Michael
last_name: Häusser
- first_name: Takuya
full_name: Notomi, Takuya
last_name: Notomi
- first_name: Yue
full_name: Wu, Yue
last_name: Wu
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Stuart
full_name: Cull Candy, Stuart
last_name: Cull Candy
citation:
ama: Momiyama A, Silver R, Häusser M, et al. The density of AMPA receptors activated
by a transmitter quantum at the climbing fibre - Purkinje cell synapse in immature
rats. Journal of Physiology. 2003;549(1):75-92. doi:10.1113/jphysiol.2002.033472
apa: Momiyama, A., Silver, R., Häusser, M., Notomi, T., Wu, Y., Shigemoto, R., &
Cull Candy, S. (2003). The density of AMPA receptors activated by a transmitter
quantum at the climbing fibre - Purkinje cell synapse in immature rats. Journal
of Physiology. Wiley. https://doi.org/10.1113/jphysiol.2002.033472
chicago: Momiyama, Akiko, Rachel Silver, Michael Häusser, Takuya Notomi, Yue Wu,
Ryuichi Shigemoto, and Stuart Cull Candy. “The Density of AMPA Receptors Activated
by a Transmitter Quantum at the Climbing Fibre - Purkinje Cell Synapse in Immature
Rats.” Journal of Physiology. Wiley, 2003. https://doi.org/10.1113/jphysiol.2002.033472.
ieee: A. Momiyama et al., “The density of AMPA receptors activated by a transmitter
quantum at the climbing fibre - Purkinje cell synapse in immature rats,” Journal
of Physiology, vol. 549, no. 1. Wiley, pp. 75–92, 2003.
ista: Momiyama A, Silver R, Häusser M, Notomi T, Wu Y, Shigemoto R, Cull Candy S.
2003. The density of AMPA receptors activated by a transmitter quantum at the
climbing fibre - Purkinje cell synapse in immature rats. Journal of Physiology.
549(1), 75–92.
mla: Momiyama, Akiko, et al. “The Density of AMPA Receptors Activated by a Transmitter
Quantum at the Climbing Fibre - Purkinje Cell Synapse in Immature Rats.” Journal
of Physiology, vol. 549, no. 1, Wiley, 2003, pp. 75–92, doi:10.1113/jphysiol.2002.033472.
short: A. Momiyama, R. Silver, M. Häusser, T. Notomi, Y. Wu, R. Shigemoto, S. Cull
Candy, Journal of Physiology 549 (2003) 75–92.
date_created: 2018-12-11T11:58:45Z
date_published: 2003-05-15T00:00:00Z
date_updated: 2026-05-22T11:31:14Z
day: '15'
doi: 10.1113/jphysiol.2002.033472
extern: '1'
external_id:
pmid:
- '12665613'
intvolume: ' 549'
issue: '1'
language:
- iso: eng
month: '05'
oa_version: None
page: 75 - 92
pmid: 1
publication: Journal of Physiology
publication_identifier:
eissn:
- 1469-7793
issn:
- 0022-3751
publication_status: published
publisher: Wiley
publist_id: '4270'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The density of AMPA receptors activated by a transmitter quantum at the climbing
fibre - Purkinje cell synapse in immature rats
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 549
year: '2003'
...
---
_id: '3799'
abstract:
- lang: eng
text: 'GABAergic interneurones are diverse in their morphological and functional
properties. Perisomatic inhibitory cells show fast spiking during sustained current
injection, whereas dendritic inhibitory cells fire action potentials with lower
frequency. We examined functional and molecular properties of K(+) channels in
interneurones with horizontal dendrites in stratum oriens-alveus (OA) of the hippocampal
CA1 region, which mainly comprise somatostatin-positive dendritic inhibitory cells.
Voltage-gated K(+) currents in nucleated patches isolated from OA interneurones
consisted of three major components: a fast delayed rectifier K(+) current component
that was highly sensitive to external 4-aminopyridine (4-AP) and tetraethylammonium
(TEA) (half-maximal inhibitory concentrations < 0.1 mM for both blockers),
a slow delayed rectifier K(+) current component that was sensitive to high concentrations
of TEA, but insensitive to 4-AP, and a rapidly inactivating A-type K(+) current
component that was blocked by high concentrations of 4-AP, but resistant to TEA.
The relative contributions of these components to the macroscopic K(+) current
were estimated as 57 +/- 5, 25 +/- 6, and 19 +/- 2 %, respectively. Dendrotoxin,
a selective blocker of Kv1 channels had only minimal effects on K(+) currents
in nucleated patches. Coapplication of the membrane-permeant cAMP analogue 8-(4-chlorophenylthio)-adenosine
3'':5''-cyclic monophosphate (cpt-cAMP) and the phosphodiesterase blocker isobutyl-methylxanthine
(IBMX) resulted in a selective inhibition of the fast delayed rectifier K(+) current
component. This inhibition was absent in the presence of the protein kinase A
(PKA) inhibitor H-89, implying the involvement of PKA-mediated phosphorylation.
Single-cell reverse transcription-polymerase chain reaction (RT-PCR) analysis
revealed a high abundance of Kv3.2 mRNA in OA interneurones, whereas the expression
level of Kv3.1 mRNA was markedly lower. Similarly, RT-PCR analysis showed a high
abundance of Kv4.3 mRNA, whereas Kv4.2 mRNA was undetectable. This suggests that
the fast delayed rectifier K(+) current and the A-type K(+) current component
are mediated predominantly by homomeric Kv3.2 and Kv4.3 channels. Selective modulation
of Kv3.2 channels in OA interneurones by cAMP is likely to be an important factor
regulating the activity of dendritic inhibitory cells in principal neurone-interneurone
microcircuits.'
acknowledgement: We thank Drs J. Bischofberger, M. Heckmann, and I. Vida for critically
reading the manuscript, and A. Blomenkamp and K. Winterhalter for technical assistance.
This work was supported by a scholarship from the Deutscher Akademischer Austansch
dienst to C.-C. L., a Deutsche Forschungsgemeinschaft grant to P. J. (SFB 505/C5),
and the Alexander-von-Humboldt foundation.
article_processing_charge: No
article_type: original
author:
- first_name: Cheng
full_name: Lien, Cheng
last_name: Lien
- first_name: Marco
full_name: Martina, Marco
last_name: Martina
- first_name: Jobst
full_name: Schultz, Jobst
last_name: Schultz
- first_name: Heimo
full_name: Ehmke, Heimo
last_name: Ehmke
- 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: Lien C, Martina M, Schultz J, Ehmke H, Jonas PM. Gating, modulation and subunit
composition of voltage-gated K(+) channels in dendritic inhibitory interneurones
of rat hippocampus. Journal of Physiology. 2002;538(Pt 2):405-419. doi:10.1113/jphysiol.2001.013066
apa: Lien, C., Martina, M., Schultz, J., Ehmke, H., & Jonas, P. M. (2002). Gating,
modulation and subunit composition of voltage-gated K(+) channels in dendritic
inhibitory interneurones of rat hippocampus. Journal of Physiology. Wiley-Blackwell.
https://doi.org/10.1113/jphysiol.2001.013066
chicago: Lien, Cheng, Marco Martina, Jobst Schultz, Heimo Ehmke, and Peter M Jonas.
“Gating, Modulation and Subunit Composition of Voltage-Gated K(+) Channels in
Dendritic Inhibitory Interneurones of Rat Hippocampus.” Journal of Physiology.
Wiley-Blackwell, 2002. https://doi.org/10.1113/jphysiol.2001.013066.
ieee: C. Lien, M. Martina, J. Schultz, H. Ehmke, and P. M. Jonas, “Gating, modulation
and subunit composition of voltage-gated K(+) channels in dendritic inhibitory
interneurones of rat hippocampus,” Journal of Physiology, vol. 538, no.
Pt 2. Wiley-Blackwell, pp. 405–419, 2002.
ista: Lien C, Martina M, Schultz J, Ehmke H, Jonas PM. 2002. Gating, modulation
and subunit composition of voltage-gated K(+) channels in dendritic inhibitory
interneurones of rat hippocampus. Journal of Physiology. 538(Pt 2), 405–419.
mla: Lien, Cheng, et al. “Gating, Modulation and Subunit Composition of Voltage-Gated
K(+) Channels in Dendritic Inhibitory Interneurones of Rat Hippocampus.” Journal
of Physiology, vol. 538, no. Pt 2, Wiley-Blackwell, 2002, pp. 405–19, doi:10.1113/jphysiol.2001.013066.
short: C. Lien, M. Martina, J. Schultz, H. Ehmke, P.M. Jonas, Journal of Physiology
538 (2002) 405–419.
date_created: 2018-12-11T12:05:14Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-11T12:32:26Z
day: '01'
doi: 10.1113/jphysiol.2001.013066
extern: '1'
external_id:
pmid:
- '11790809'
intvolume: ' 538'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290075/
month: '01'
oa: 1
oa_version: Published Version
page: 405 - 419
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2411'
quality_controlled: '1'
status: public
title: Gating, modulation and subunit composition of voltage-gated K(+) channels in
dendritic inhibitory interneurones of rat hippocampus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 538
year: '2002'
...
---
_id: '3801'
abstract:
- lang: eng
text: 'To examine possible interactions between fast depression and modulation of
inhibitory synaptic transmission in the hippocampus, we recorded from pairs of
synaptically connected basket cells (BCs) and granule cells (GCs) in the dentate
gyrus of rat brain slices at 34 degrees C. Multiple-pulse depression (MPD) was
examined in trains of 5 or 10 inhibitory postsynaptic currents (IPSCs) evoked
at frequencies of 10-100 Hz under several conditions that inhibit transmitter
release: block of voltage-dependent Ca2+ channels by Cd2+ (10 microM), activation
of gamma-amino-butyric acid type B receptors (GABA(B)Rs) by baclofen (10 microM)
and activation of muscarinic acetylcholine receptors (mAchRs) by carbachol (2
microM). All manipulations led to a substantial inhibition of synaptic transmission,
reducing the amplitude of the first IPSC in the train (IPSC1) by 72%, 61% and
29%, respectively. However, MPD was largely preserved under these conditions (0.34
in control versus 0.31, 0.50 and 0.47 in the respective conditions at 50 Hz).
Similarly, a theta burst stimulation (TBS) protocol reduced IPSC1 by 54%, but
left MPD unchanged (0.40 in control and 0.39 during TBS). Analysis of both fractions
of transmission failures and coefficients of variation (CV) of IPSC peak amplitudes
suggested that MPD had a presynaptic expression site, independent of release probability.
In conclusion, different types of presynaptic modulation of inhibitory synaptic
transmission converge on a reduction of synaptic strength, while short-term dynamics
are largely unchanged.'
acknowledgement: We thank Drs M. Bartos, J. Bischofberger, M. Heckmann and
I. Vida for critically reading the manuscript, Dr K. Götz for providing information about pharmacological properties of
inhibitory hippocampal synapses, and A. Blomenkamp and K. Winterhalter for
technical assistance. This work was supported by Deutsche Forschungsgemeinschaft
grants to P.J. (Jo-248/2-2,SFB 505/C5) and the Alexander-von-Humboldt foundation.
article_processing_charge: No
article_type: original
author:
- first_name: Stefan
full_name: Hefft, Stefan
last_name: Hefft
- first_name: Udo
full_name: Kraushaar, Udo
last_name: Kraushaar
- first_name: Jörg
full_name: Geiger, Jörg
last_name: Geiger
- 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: Hefft S, Kraushaar U, Geiger J, Jonas PM. Presynaptic short-term depression
is maintained during regulation of transmitter release at a GABAergic synapse
in rat hippocampus. Journal of Physiology. 2002;539(Pt 1):201-208. doi:10.1113/jphysiol.2001.013455
apa: Hefft, S., Kraushaar, U., Geiger, J., & Jonas, P. M. (2002). Presynaptic
short-term depression is maintained during regulation of transmitter release at
a GABAergic synapse in rat hippocampus. Journal of Physiology. Wiley-Blackwell.
https://doi.org/10.1113/jphysiol.2001.013455
chicago: Hefft, Stefan, Udo Kraushaar, Jörg Geiger, and Peter M Jonas. “Presynaptic
Short-Term Depression Is Maintained during Regulation of Transmitter Release at
a GABAergic Synapse in Rat Hippocampus.” Journal of Physiology. Wiley-Blackwell,
2002. https://doi.org/10.1113/jphysiol.2001.013455.
ieee: S. Hefft, U. Kraushaar, J. Geiger, and P. M. Jonas, “Presynaptic short-term
depression is maintained during regulation of transmitter release at a GABAergic
synapse in rat hippocampus,” Journal of Physiology, vol. 539, no. Pt 1.
Wiley-Blackwell, pp. 201–8, 2002.
ista: Hefft S, Kraushaar U, Geiger J, Jonas PM. 2002. Presynaptic short-term depression
is maintained during regulation of transmitter release at a GABAergic synapse
in rat hippocampus. Journal of Physiology. 539(Pt 1), 201–8.
mla: Hefft, Stefan, et al. “Presynaptic Short-Term Depression Is Maintained during
Regulation of Transmitter Release at a GABAergic Synapse in Rat Hippocampus.”
Journal of Physiology, vol. 539, no. Pt 1, Wiley-Blackwell, 2002, pp. 201–08,
doi:10.1113/jphysiol.2001.013455.
short: S. Hefft, U. Kraushaar, J. Geiger, P.M. Jonas, Journal of Physiology 539
(2002) 201–8.
date_created: 2018-12-11T12:05:15Z
date_published: 2002-02-01T00:00:00Z
date_updated: 2023-07-11T10:01:12Z
day: '01'
doi: 10.1113/jphysiol.2001.013455
extern: '1'
external_id:
pmid:
- '11850513'
intvolume: ' 539'
issue: Pt 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290140/
month: '02'
oa: 1
oa_version: Published Version
page: 201 - 8
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2410'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Presynaptic short-term depression is maintained during regulation of transmitter
release at a GABAergic synapse in rat hippocampus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 539
year: '2002'
...
---
_id: '3485'
abstract:
- lang: eng
text: 1. GABAergic interneurones differ from glutamatergic principal neurones in
their ability to discharge high-frequency trains of action potentials without
adaptation. To examine whether Na+ channel gating contributed to these differences,
Na+ currents were recorded in nucleated patches from interneurones (dentate gyrus
basket cells, BCs) and principal neurones (CA1 pyramidal cells, PCs) of rat hippocampal
slices. 2. The voltage dependence of Na+ channel activation in BCs and PCs was
similar. The slope factors of the activation curves, fitted with Boltzmann functions
raised to the third power, were 11.5 and 11.8 mV, and the mid-point potentials
were -25.1 and -23.9 mV, respectively. 3. Whereas the time course of Na+ channel
activation (-30 to +40 mV) was similar, the deactivation kinetics (-100 to -40
mV) were faster in BCs than in PCs (tail current decay time constants, 0.13 and
0.20 ms, respectively, at -40 mV). 4. Na+ channels in BCs and PCs differed in
the voltage dependence of inactivation. The slope factors of the steady-state
inactivation curves fitted with Boltzmann functions were 6.7 and 10.7 mV, and
the mid-point potentials were -58.3 and -62.9 mV, respectively. 5. The onset of
Na+ channel inactivation at -55 mV was slower in BC's than in PCs; the inactivation
time constants were 18.6 and 9.3 ms, respectively. At more positive potentials
the differences in inactivation onset were smaller. 6. The time course of recovery
of Na+ channels from inactivation induced by a 30 ms pulse was fast and mono-exponential
(τ = 2.0 ms at -120 mV) in BCs, whereas it was slower and biexponential in PCs
(τ1 = 2.0 ms and τ2 = 133 ms; amplitude contribution of the slow component, 15%).
7. We conclude that Na+ channels of BCs and PCs differ in gating properties that
contribute to the characteristic action potential patterns of the two types of
neurones.
acknowledgement: We thank Drs J. Bischofberger and J. R. P. Geiger for critically
reading the manuscript, Mrs B. Plessow-Freudenberg and K. Zipfel for technical assistance,
and Mrs B. Hillers for typing. This work was supported by the German Israeli Foundation
grant I 0352–073.01/94 to P. J.
article_processing_charge: No
article_type: original
author:
- first_name: Marco
full_name: Martina, Marco
last_name: Martina
- 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: Martina M, Jonas PM. Functional differences in Na+ channel gating between fast-spiking
interneurones and principal neurones in rat hippocampus. Journal of Physiology.
1997;505(3):593-603. doi:10.1111/j.1469-7793.1997.593ba.x
apa: Martina, M., & Jonas, P. M. (1997). Functional differences in Na+ channel
gating between fast-spiking interneurones and principal neurones in rat hippocampus.
Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1111/j.1469-7793.1997.593ba.x
chicago: Martina, Marco, and Peter M Jonas. “Functional Differences in Na+ Channel
Gating between Fast-Spiking Interneurones and Principal Neurones in Rat Hippocampus.”
Journal of Physiology. Wiley-Blackwell, 1997. https://doi.org/10.1111/j.1469-7793.1997.593ba.x.
ieee: M. Martina and P. M. Jonas, “Functional differences in Na+ channel gating
between fast-spiking interneurones and principal neurones in rat hippocampus,”
Journal of Physiology, vol. 505, no. 3. Wiley-Blackwell, pp. 593–603, 1997.
ista: Martina M, Jonas PM. 1997. Functional differences in Na+ channel gating between
fast-spiking interneurones and principal neurones in rat hippocampus. Journal
of Physiology. 505(3), 593–603.
mla: Martina, Marco, and Peter M. Jonas. “Functional Differences in Na+ Channel
Gating between Fast-Spiking Interneurones and Principal Neurones in Rat Hippocampus.”
Journal of Physiology, vol. 505, no. 3, Wiley-Blackwell, 1997, pp. 593–603,
doi:10.1111/j.1469-7793.1997.593ba.x.
short: M. Martina, P.M. Jonas, Journal of Physiology 505 (1997) 593–603.
date_created: 2018-12-11T12:03:34Z
date_published: 1997-12-15T00:00:00Z
date_updated: 2022-08-22T08:25:26Z
day: '15'
doi: 10.1111/j.1469-7793.1997.593ba.x
extern: '1'
external_id:
pmid:
- '9457638'
intvolume: ' 505'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1160038/
month: '12'
oa: 1
oa_version: Published Version
page: 593 - 603
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2902'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Functional differences in Na+ channel gating between fast-spiking interneurones
and principal neurones in rat hippocampus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 505
year: '1997'
...
---
_id: '3486'
abstract:
- lang: eng
text: 1. Dendritic patch-clamp recordings were obtained from mitral cells in rat
olfactory bulb slices, up to 350 μm from the soma. Simultaneous dendritic and
somatic whole-cell recordings indicated that action potentials (APs) evoked by
somatic or dendritic current injection were initiated near the soma. Both the
large amplitude (100.7 ± 1.1 mV) and the short duration (1.38 ± 0.07 ms) of the
AP were maintained as the AP propagated back into the primary mitral cell dendrites.
2. Outside-out patches isolated from mitral cell dendrites contained voltage-gated
Na+ channels (peak conductance density, 90 pS μm-2 at -10 mV). When an AP was
used as a somatic voltage-clamp command in the presence of 1 μM tetrodotoxin (TTX),
the amplitude of the dendritic potential was attenuated to 48 ± 14 mV. This shows
that dendritic Na+ channels support the active back-propagation of APs. 3. Dendritic
patches contained voltage-gated K+ channels with high density (conductance density,
513 pS μm-2 at 30 mV. Dendritic K+ currents were reduced to 35% by 1 mM external
tetraethylammonium chloride (TEACl). When an AP was used as a somatic voltage
clamp command in the presence of TEACl, the dendritic potential was markedly prolonged.
This indicates that dendritic K+ channels mediate the fast repolarization of dendritic
APs. 4. We conclude that voltage gated Na+ and K+ channels support dendritic APs
with large amplitudes and short durations that may trigger fast transmitter release
at dendrodendritic synapses in the olfactory bulb.
acknowledgement: We thank Drs J. R. P. Geiger, M. Martina, and D. Schild for critically
reading the manuscript, and Mrs B. Plessow-Freudenberg for technical assistance.
This work was supported by DFG grant BI 642/1-1 and German Israeli Foundation grant
I 0352-073.01/94.
article_processing_charge: No
article_type: original
author:
- first_name: Joseph
full_name: Bischofberger, Joseph
last_name: Bischofberger
- 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: Bischofberger J, Jonas PM. Action potential propagation into the presynaptic
dendrites of rat mitral cells. Journal of Physiology. 1997;504(Pt 2):359-365.
doi:10.1111/j.1469-7793.1997.359be.x
apa: Bischofberger, J., & Jonas, P. M. (1997). Action potential propagation
into the presynaptic dendrites of rat mitral cells. Journal of Physiology.
Wiley-Blackwell. https://doi.org/10.1111/j.1469-7793.1997.359be.x
chicago: Bischofberger, Joseph, and Peter M Jonas. “Action Potential Propagation
into the Presynaptic Dendrites of Rat Mitral Cells.” Journal of Physiology.
Wiley-Blackwell, 1997. https://doi.org/10.1111/j.1469-7793.1997.359be.x.
ieee: J. Bischofberger and P. M. Jonas, “Action potential propagation into the presynaptic
dendrites of rat mitral cells,” Journal of Physiology, vol. 504, no. Pt
2. Wiley-Blackwell, pp. 359–365, 1997.
ista: Bischofberger J, Jonas PM. 1997. Action potential propagation into the presynaptic
dendrites of rat mitral cells. Journal of Physiology. 504(Pt 2), 359–365.
mla: Bischofberger, Joseph, and Peter M. Jonas. “Action Potential Propagation into
the Presynaptic Dendrites of Rat Mitral Cells.” Journal of Physiology,
vol. 504, no. Pt 2, Wiley-Blackwell, 1997, pp. 359–65, doi:10.1111/j.1469-7793.1997.359be.x.
short: J. Bischofberger, P.M. Jonas, Journal of Physiology 504 (1997) 359–365.
date_created: 2018-12-11T12:03:35Z
date_published: 1997-10-15T00:00:00Z
date_updated: 2022-08-19T12:02:21Z
day: '15'
doi: 10.1111/j.1469-7793.1997.359be.x
extern: '1'
external_id:
pmid:
- '9365910'
intvolume: ' 504'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1159916/
month: '10'
oa: 1
oa_version: Published Version
page: 359 - 365
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2901'
quality_controlled: '1'
status: public
title: Action potential propagation into the presynaptic dendrites of rat mitral cells
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 504
year: '1997'
...
---
_id: '3478'
abstract:
- lang: eng
text: 1. Properties of dendritic glutamate receptor (GluR) channels were investigated
using fast application of glutamate to outside-out membrane patches isolated from
the apical dendrites of CA3 and CA1 pyramidal neurons in rat hippocampal slices.
CA3 patches were formed (15-76 μm from the soma) in the region of messy fibre
(MF) synapses, and CA1 patches (25-174 μm from the soma) in the region of Schaffer
collateral (SC) innervation. 2. Dual-component responses consisting of a rapidly
rising and decaying component followed by a second, substantially slower, component
were elicited by 1 ms pulses of 1 mM glutamate in the presence of 10 μM glycine
and absence of external Mg2+. The fast component was selectively blocked by 2-5
μM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the slow component by 30 μM
D-2-amino-5-phosphonopentanoic acid (D-AP5), suggesting that the fast and slow
components were mediated by the GluR channels of the L-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate
(AMPA) and NMDA type, respectively. The peak amplitude ratio of the NMDA to AMPA
receptor-mediated components varied between 0.03 and 0.62 in patches from both
CA3 and CA1 dendrites. Patches lacking either component were rarely observed.
3. The peak current-voltage (I-V) relationship of the fast component was almost
linear, whereas the I-V relationship of the slow component showed a region of
negative slope in the presence of 1 mM external Mg2+. The reversal potential for
both components was close to 0 mV. 4. Kainate-preferring GluR channels did not
contribute appreciably to the response to glutamate. The responses to 100 ms pulses
of 1 mM glutamate were mimicked by application of 1 mM AMPA, whereas 1 mM kainate
produced much smaller, weakly desensitizing currents. This suggests that the fast
component is primarily mediated by the action of glutamate on AMPA-preferring
receptors. 5. The mean elementary conductance of AMPA receptor channels was about
10 pS, as estimated by non-stationary fluctuation analysis. The permeability of
these channels to Ca2+ was low (~5% of the permeability to Cs+). 6. The elementary
conductance of NMDA receptor channels was larger, with a main conductance state
of about 45 pS. These channels were 3.6 times more permeable to Ca2+ than to Cs+.
7. AMPA receptor-mediated currents activated rapidly in response to 1 ms pulses
of 1 mM glutamate and deactivated with a predominant, fast time constant and a
smaller, slower component (τ1≃2 ms, τ2≃8 ms, contributing ~80 and ~20% to the
total decay amplitude, respectively). Desensitization of the current during a
100 ms pulse was best fitted by two time constants (τ1≃10 ms, ~60%; τ2≃34 ms,
~40%). 8. NMDA receptor-mediated currents in response to 1 ms pulses of 1 mM glutamate
activated and deactivated much more slowly than AMPA receptor-mediated currents.
The time course could be described by a single exponential rising phase (τ≃7 ms)
followed by a double exponential decay (τ1≃200 ms, ~80%; τ2≃1-3 s, ~20%). 9. Mg2+
blocked the NMDA component in a voltage-dependent manner, with a half-maximal
inhibitory concentration (IC50) of 21 μM at -80 mV. At physiological Mg2+ concentrations,
block of the NMDA component could be rapidly relieved with voltage jumps from
negative to positive potentials. Block of the current upon return to negative
potentials occurred almost instantaneously. 10. Zn2+ also selectively-blocked
the NMDA receptor-mediated current with an IC50 of 22 μM, but this block differed
from that of Mg2+ in that it showed little voltage dependence. Rapid application
of Zn2+ together with glutamate produced partial block of the current. More block
was observed if Zn2+ and glutamate were co-applied when NMDA receptor channels
were already open. 11. The functional properties of dendritic GluRs were similar
to those found at the soma. Knowledge of these properties facilitated simulations
investigating the contribution of coactivated AMPA and NMDA receptors to synaptic
depolarization and Ca2+ entry into dendritic spines. Because of its slow deactivation,
the NMDA receptor-mediated current contributes substantially to depolarization
and Ca2+ entry and is susceptible to modulation over a period of seconds, either
by backpropagating action potentials or by the release of Zn2+ from presynaptic
boutons.
acknowledgement: We thank M.Hausser, A.Roth, P.Ruppersberg, and G.Stuart for helpful
discussions and M.H. and G.S. for critically reading the manuscript. We also thank
M.Kaiser for expert technical assistance and F.Helmchen, M.Huke and A.Roth for computer
programming. Financial support from the Alexander von Humboldt Foundation and the
Deutsche Forschungsgemeinschaft (SFB317) is gratefully acknowledged.
article_processing_charge: No
article_type: original
author:
- first_name: Nelson
full_name: Spruston, Nelson
last_name: Spruston
- 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: Bert
full_name: Sakmann, Bert
last_name: Sakmann
citation:
ama: Spruston N, Jonas PM, Sakmann B. Dendritic glutamate receptor channels in rat
hippocampal CA3 and CA1 pyramidal neurons. Journal of Physiology. 1995;482(Pt
2):325-352. doi:10.1113/jphysiol.1995.sp020521
apa: Spruston, N., Jonas, P. M., & Sakmann, B. (1995). Dendritic glutamate receptor
channels in rat hippocampal CA3 and CA1 pyramidal neurons. Journal of Physiology.
Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1995.sp020521
chicago: Spruston, Nelson, Peter M Jonas, and Bert Sakmann. “Dendritic Glutamate
Receptor Channels in Rat Hippocampal CA3 and CA1 Pyramidal Neurons.” Journal
of Physiology. Wiley-Blackwell, 1995. https://doi.org/10.1113/jphysiol.1995.sp020521.
ieee: N. Spruston, P. M. Jonas, and B. Sakmann, “Dendritic glutamate receptor channels
in rat hippocampal CA3 and CA1 pyramidal neurons,” Journal of Physiology,
vol. 482, no. Pt 2. Wiley-Blackwell, pp. 325–352, 1995.
ista: Spruston N, Jonas PM, Sakmann B. 1995. Dendritic glutamate receptor channels
in rat hippocampal CA3 and CA1 pyramidal neurons. Journal of Physiology. 482(Pt
2), 325–352.
mla: Spruston, Nelson, et al. “Dendritic Glutamate Receptor Channels in Rat Hippocampal
CA3 and CA1 Pyramidal Neurons.” Journal of Physiology, vol. 482, no. Pt
2, Wiley-Blackwell, 1995, pp. 325–52, doi:10.1113/jphysiol.1995.sp020521.
short: N. Spruston, P.M. Jonas, B. Sakmann, Journal of Physiology 482 (1995) 325–352.
date_created: 2018-12-11T12:03:32Z
date_published: 1995-01-15T00:00:00Z
date_updated: 2022-06-28T08:08:40Z
day: '15'
doi: 10.1113/jphysiol.1995.sp020521
extern: '1'
external_id:
pmid:
- '7536248'
intvolume: ' 482'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.1995.sp020521
month: '01'
oa: 1
oa_version: Published Version
page: 325 - 352
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2909'
quality_controlled: '1'
status: public
title: Dendritic glutamate receptor channels in rat hippocampal CA3 and CA1 pyramidal
neurons
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 482
year: '1995'
...
---
_id: '3479'
abstract:
- lang: eng
text: 1. Glutamate receptor (GluR) channels were studied in basket cells in the
dentate gyrus of rat hippocampal slices. Basket cells were identified by their
location, dendritic morphology and high frequency of action potentials generated
during sustained current injection. 2. Dual-component currents were activated
by fast application of glutamate to outside-out membrane patches isolated from
basket cell somata (10 μM glycine, no external Mg2+). The fast component was selectively
blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the slow component by
D-2-amino-5-phosphonopentanoic acid (D-AP5). This suggests that the two components
were mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor (AMPAR)/kainate
receptor and N-methyl-D-aspartate receptor (NMDAR) channels, respectively. The
mean ratio of the peak current of the NMDAR component to that of the AMPAR/kainate
receptor component was 0.22 (1 ms pulses of 10 mM glutamate). 3. The AMPAR/kainate
receptor component, which was studied in isolation in the presence of D-AP5, was
identified as AMPAR mediated on the basis of the preferential activation by AMPA
as compared with kainate, the weak desensitization of kainate-activated currents,
the cross-desensitization between AMPA and kainate, and the reduction of desensitization
by cyclothiazide. 4. Deactivation of basket cell AMPARs following 1 ms pulses
of glutamate occurred with a time constant (τ) of 1.2 ± 0.1 ms (mean ± S.E.M.).
During 100 ms glutamate pulses, AMPARs desensitized with a τ of 3.7 ± 0.2 ms.
5. The peak current-voltage (I-V) relation of AMPAR-mediated currents in Na+-rich
extracellular solution showed a reversal potential of -4.0 ± 2.6 mV and was characterized
by a doubly rectifying shape. The conductance of single AMPAR channels was estimated
as 22.6 ± 1.6 pS using non-stationary fluctuation analysis. AMPARs expressed in
hippocampal basket cells mere highly Ca2+ permeable (P(Ca)/P(K) = 1.79). 6. NMDARs
in hippocampal basket cells were studied in isolation in the presence of CNQX.
Deactivation of NMDARs activated by glutamate pulses occurred bi-exponentially
with mean τ values of 266 ± 23 ms (76%) and 2620 ± 383 ms (24%). 7. The peak I-V
relation of the NMDAR-mediated component in Na+-rich extracellular solution showed
a reversal potential of 1.5 ± 0.6 mV and a region of negative slope at negative
membrane potentials in the presence of external Mg2+, due to voltage-dependent
block by these ions. The conductance of single NMDAR channels in the main open
state was 50.2 ± 1.8 pS. NMDARs in hippocampal basket cells were highly permeable
to Ca2+ (P(Ca)/P(K) = 6.68). 8. AMPARs in hippocampal basket cells are characterized
by about threefold faster kinetics and twentyfold higher Ca2+ permeability than
AMPARs in hippocampal granule or pyramidal cells. Simulations show that the Ca2+
influx through basket cell AMPARs is comparable to that through NMDARs at negative
membrane potentials with physiological concentrations of Ca2+ and Mg2+. This suggests
a dual pathway of synaptically mediated Ca2+ entry into interneurones.
acknowledgement: We thank Drs M.Häusser and H.Markram for critically reading the manuscript
and M.Kaiser for technical assistance. Supported by the Deutsche Forschungsgemeinschaft
(SFB-317/B14 grant to P.J. and a Graduiertenkollegstipendium to J.R.P.G.)
article_processing_charge: No
article_type: original
author:
- first_name: Duk
full_name: Koh, Duk
last_name: Koh
- first_name: Jörg
full_name: Geiger, Jörg
last_name: Geiger
- 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: Bert
full_name: Sakmann, Bert
last_name: Sakmann
citation:
ama: Koh D, Geiger J, Jonas PM, Sakmann B. Ca(2+)-permeable AMPA and NMDA receptor
channels in basket cells of rat hippocampal dentate gyrus. Journal of Physiology.
1995;485(Pt 2):383-402. doi:10.1113/jphysiol.1995.sp020737
apa: Koh, D., Geiger, J., Jonas, P. M., & Sakmann, B. (1995). Ca(2+)-permeable
AMPA and NMDA receptor channels in basket cells of rat hippocampal dentate gyrus.
Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1995.sp020737
chicago: Koh, Duk, Jörg Geiger, Peter M Jonas, and Bert Sakmann. “Ca(2+)-Permeable
AMPA and NMDA Receptor Channels in Basket Cells of Rat Hippocampal Dentate Gyrus.”
Journal of Physiology. Wiley-Blackwell, 1995. https://doi.org/10.1113/jphysiol.1995.sp020737.
ieee: D. Koh, J. Geiger, P. M. Jonas, and B. Sakmann, “Ca(2+)-permeable AMPA and
NMDA receptor channels in basket cells of rat hippocampal dentate gyrus,” Journal
of Physiology, vol. 485, no. Pt 2. Wiley-Blackwell, pp. 383–402, 1995.
ista: Koh D, Geiger J, Jonas PM, Sakmann B. 1995. Ca(2+)-permeable AMPA and NMDA
receptor channels in basket cells of rat hippocampal dentate gyrus. Journal of
Physiology. 485(Pt 2), 383–402.
mla: Koh, Duk, et al. “Ca(2+)-Permeable AMPA and NMDA Receptor Channels in Basket
Cells of Rat Hippocampal Dentate Gyrus.” Journal of Physiology, vol. 485,
no. Pt 2, Wiley-Blackwell, 1995, pp. 383–402, doi:10.1113/jphysiol.1995.sp020737.
short: D. Koh, J. Geiger, P.M. Jonas, B. Sakmann, Journal of Physiology 485 (1995)
383–402.
date_created: 2018-12-11T12:03:33Z
date_published: 1995-06-01T00:00:00Z
date_updated: 2022-06-28T07:54:44Z
day: '01'
doi: 10.1113/jphysiol.1995.sp020737
extern: '1'
external_id:
pmid:
- '7545230'
intvolume: ' 485'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1158000/pdf/jphysiol00319-0104.pdf
month: '06'
oa: 1
oa_version: Published Version
page: 383 - 402
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2908'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ca(2+)-permeable AMPA and NMDA receptor channels in basket cells of rat hippocampal
dentate gyrus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 485
year: '1995'
...
---
_id: '3481'
abstract:
- lang: eng
text: 1. The influence of intracellular factors on current rectification of different
subtypes of native α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors
(AMPARs) was studied in rat brain slices by combining fast application of glutamate
with patch pipette perfusion. 2. The peak current-voltage (I-V) relation of the
AMPARs expressed in Bergmann glial cells of cerebellum and dentate gyrus (DG)
basket cells of hippocampus was weakly rectifying in outside-out patches and nystatin-perforated
vesicles, but showed a doubly rectifying shape with a region of reduced slope
between 0 and +40 mV in nucleated patches. The I-V relation of AMPARs expressed
in hippocampal CA3 pyramidal neurones was linear in all recording configurations.
3. Intracellular application of 2.5 μM spermine, a naturally occurring polyamine,
blocked outward currents in outside-oat patches from Bergmann glial cells and
DG basket cells in a voltage-dependent manner, generating I-V relations with a
doubly rectifying shape which were similar to those recorded in nucleated patches.
AMPARs in CA3 pyramidal cell patches were unaffected by 25 μM spermine. 4. The
half-maximal blocking concentration of spermine at +40 mV was 0.3 μM in Bergmann
glial cell patches and 1.5 μM in DG basket cell patches, whereas it was much higher
(≥ 100 μM) for CA3 pyramidal. cell patches. Spermidine also affected current rectification,
but with lower affinity. The block of outward current by polyamines following
voltage jumps developed within < 0.5 ms. 5. We conclude that current rectification,
rather than being an intrinsic property of the Ca2+ permeable AMPAR channel, is
generated by polyamine block.
acknowledgement: We thank Dr B.Sakmann, Dr V.Witzemann, J.Geiger, and A.Roth for helpful
discussions and Dr D.Feldmeyer and Dr A.Villarroel for reading the manuscript. We
also thank M.Kaiser for technical and H.Spiegel for secretarial assistance. Supported
by DFG grant SFB-317/B14(P.J.).
article_processing_charge: No
article_type: original
author:
- first_name: Duk
full_name: Koh, Duk
last_name: Koh
- first_name: Nail
full_name: Burnashev, Nail
last_name: Burnashev
- 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: Koh D, Burnashev N, Jonas PM. Block of native Ca(2+)-permeable AMPA receptors
in rat brain by intracellular polyamines generates double rectification. Journal
of Physiology. 1995;486(Pt 2):305-312. doi:10.1113/jphysiol.1995.sp020813
apa: Koh, D., Burnashev, N., & Jonas, P. M. (1995). Block of native Ca(2+)-permeable
AMPA receptors in rat brain by intracellular polyamines generates double rectification.
Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1995.sp020813
chicago: Koh, Duk, Nail Burnashev, and Peter M Jonas. “Block of Native Ca(2+)-Permeable
AMPA Receptors in Rat Brain by Intracellular Polyamines Generates Double Rectification.”
Journal of Physiology. Wiley-Blackwell, 1995. https://doi.org/10.1113/jphysiol.1995.sp020813.
ieee: D. Koh, N. Burnashev, and P. M. Jonas, “Block of native Ca(2+)-permeable AMPA
receptors in rat brain by intracellular polyamines generates double rectification,”
Journal of Physiology, vol. 486, no. Pt 2. Wiley-Blackwell, pp. 305–312,
1995.
ista: Koh D, Burnashev N, Jonas PM. 1995. Block of native Ca(2+)-permeable AMPA
receptors in rat brain by intracellular polyamines generates double rectification.
Journal of Physiology. 486(Pt 2), 305–312.
mla: Koh, Duk, et al. “Block of Native Ca(2+)-Permeable AMPA Receptors in Rat Brain
by Intracellular Polyamines Generates Double Rectification.” Journal of Physiology,
vol. 486, no. Pt 2, Wiley-Blackwell, 1995, pp. 305–12, doi:10.1113/jphysiol.1995.sp020813.
short: D. Koh, N. Burnashev, P.M. Jonas, Journal of Physiology 486 (1995) 305–312.
date_created: 2018-12-11T12:03:33Z
date_published: 1995-07-15T00:00:00Z
date_updated: 2022-06-27T14:53:16Z
day: '15'
doi: 10.1113/jphysiol.1995.sp020813
extern: '1'
external_id:
pmid:
- '7473198'
intvolume: ' 486'
issue: Pt 2
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1156754/
month: '07'
oa: 1
oa_version: Published Version
page: 305 - 312
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2906'
quality_controlled: '1'
status: public
title: Block of native Ca(2+)-permeable AMPA receptors in rat brain by intracellular
polyamines generates double rectification
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 486
year: '1995'
...
---
_id: '3475'
abstract:
- lang: eng
text: '1. A potassium channel activated by internal Na+ ions (K+Na channel) was
identified in peripheral myelinated axons of Xenopus laevis using the cell-attached
and excised configurations of the patch clamp technique. 2. The single-channel
conductance for the main open state was 88 pS with [K+]o = 105 mM and pS with
[K+]o = 2.5 mM ([K+]i = 105 mM). The channel was selectively permeable to K+ over
Na+ ions. A characteristic feature of the K+Na channel was the frequent occurrence
of subconductance states. 3. The open probability of the channel was strongly
dependent on the concentration of Na+ ions at the inner side of the membrane.
The half-maximal activating Na+ concentration and the Hill coefficient were 33
mM and 2.9, respectively. The open probability of the channel showed only weak
potential dependence. 4. The K+Na channel was relatively insensitive to external
tetraethylammonium (TEA+) in comparison with voltage-dependent axonal K+ channels;
the half-maximal inhibitory concentration (IC50) was 21.3 mM (at -90 mV). In contrast,
the channel was blocked by low concentrations of external Ba2+ and Cs+ ions, with
IC50 values of 0.7 and 1.1 mM, respectively (at -90 mV). The block by Ba2+ and
Cs+ was more pronounced at negative than at positive membrane potentials. 5. A
comparison of the number of K+Na channels in nodal and paranodal patches from
the same axon revealed that the channel density was about 10-fold higher at the
node of Ranvier than at the paranode. Moreover, a correlation between the number
of K+Na channels and voltage-dependent Na+ channels in the same patches was found,
suggesting co-localization of both channel types. 6. As weakly potential-dependent
(''leakage'') channels, axonal K+Na channels may be involved in setting the resting
potential of vertebrate axons. Simulations of Na+ ion diffusion suggest two possible
mechanisms of activation of K+Na channels: the local increase of Na+ concentration
in a cluster of Na+ channels during a single action potential or the accumulation
in the intracellular axonal compartment during a train of action potentials.'
acknowledgement: 'We thank Drs M.Häusser and A. Villarroel for critically reading
the manuscript, Dr E. v. Kitzing and A. Roth for many helpful discussions. This
work was supported by the Deutsche Forschungsgemeinschaft (Vo188/13-2). '
article_processing_charge: No
article_type: original
author:
- first_name: Duk
full_name: Koh, Duk
last_name: Koh
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Werner
full_name: Vogel, Werner
last_name: Vogel
citation:
ama: Koh D, Jonas PM, Vogel W. Na+-activated K+ channels localized in the nodal
region of myelinated axons of Xenopus. Journal of Physiology. 1994;479:183-197.
doi:10.1113/jphysiol.1994.sp020287
apa: Koh, D., Jonas, P. M., & Vogel, W. (1994). Na+-activated K+ channels localized
in the nodal region of myelinated axons of Xenopus. Journal of Physiology.
Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1994.sp020287
chicago: Koh, Duk, Peter M Jonas, and Werner Vogel. “Na+-Activated K+ Channels Localized
in the Nodal Region of Myelinated Axons of Xenopus.” Journal of Physiology.
Wiley-Blackwell, 1994. https://doi.org/10.1113/jphysiol.1994.sp020287.
ieee: D. Koh, P. M. Jonas, and W. Vogel, “Na+-activated K+ channels localized in
the nodal region of myelinated axons of Xenopus,” Journal of Physiology,
vol. 479. Wiley-Blackwell, pp. 183–197, 1994.
ista: Koh D, Jonas PM, Vogel W. 1994. Na+-activated K+ channels localized in the
nodal region of myelinated axons of Xenopus. Journal of Physiology. 479, 183–197.
mla: Koh, Duk, et al. “Na+-Activated K+ Channels Localized in the Nodal Region of
Myelinated Axons of Xenopus.” Journal of Physiology, vol. 479, Wiley-Blackwell,
1994, pp. 183–97, doi:10.1113/jphysiol.1994.sp020287.
short: D. Koh, P.M. Jonas, W. Vogel, Journal of Physiology 479 (1994) 183–197.
date_created: 2018-12-11T12:03:31Z
date_published: 1994-01-01T00:00:00Z
date_updated: 2022-06-03T11:09:21Z
day: '01'
doi: 10.1113/jphysiol.1994.sp020287
extern: '1'
external_id:
pmid:
- '7799220 '
intvolume: ' 479'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1155738/
month: '01'
oa: 1
oa_version: Published Version
page: 183 - 197
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2912'
quality_controlled: '1'
status: public
title: Na+-activated K+ channels localized in the nodal region of myelinated axons
of Xenopus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 479
year: '1994'
...
---
_id: '3474'
abstract:
- lang: eng
text: 1. Excitatory postsynaptic currents (EPSCs) were recorded in CA3 pyramidal
cells of hippocampal slices of 15- to 24-day-old rats (22 degrees C) using the
whole-cell configuration of the patch clamp technique. 2. Composite EPSCs were
evoked by extracellular stimulation of the mossy fibre tract. Using the selective
blockers 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D-2-amino-5-phosphonopentanoic
acid (APV), a major alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate
receptor-mediated component and a minor NMDA receptor-mediated component with
slower time course were distinguished. For the AMPA/kainate receptor-mediated
component, the peak current-voltage (I-V) relation was linear, with a reversal
potential close to 0 mV. The half-maximal blocking concentration of CNQX was 353
nM. 3. Unitary EPSCs of the mossy fibre terminal (MF)-CA3 pyramidal cell synapse
were evoked at membrane potentials of -70 to -90 mV by low-intensity extracellular
stimulation of granule cell somata using fine-tipped pipettes. The EPSC peak amplitude
as a function of stimulus intensity showed all-or-none behaviour. The region of
low threshold was restricted to a few micrometres. This suggests that extracellular
stimulation was focal, and that the stimulus-evoked EPSCs were unitary. 4. Latency
and rise time histograms of EPSCs evoked by granule cell stimulation showed narrow
unimodal distributions within each experiment. The mean latency was 4.2 +/- 1.0
ms, and the mean 20-80% rise time was 0.6 +/- 0.1 ms (23 cells). When fitted within
the range 0.7 ms to 20 ms after the peak, the decay of the EPSCs with the fastest
rise (rise time 0.5 ms or less) could be described by a single exponential function;
the mean time constant was in the range 3.0-6.6 ms with a mean of 4.8 ms (8 cells).
5. Peak amplitudes of the EPSCs evoked by suprathreshold granule cell stimulation
fluctuated between trials. The apparent EPSC peak conductance in normal extracellular
solution (2 mM Ca2+, 1 mM Mg2+), excluding failures, was 1 nS. Reducing the Ca2+
concentration and increasing the Mg2+ concentration reduced the mean peak amplitude
in a concentration-dependent manner. 6. Peaks in EPSC peak amplitude distributions
were apparent in low Ca2+ and high Mg2+. Using the criteria of equidistance and
the presence of peaks and dips in the autocorrelation function, five of nine EPSC
peak amplitude distributions were judged to be quantal.
acknowledgement: "We are indebted to Professor B. Katz for critically reading the
manuscript and for helpful suggestions. We especially thank Professor D. Colquhoun
for several discussions, for generously providing the source codes of programs for
maximum-likelihood fit with sums of Gaussian functions, a routine for calculating
the error function and for critically reading the manuscript. We also thank Drs
A. Larkman, P. Ruppersberg, N. Spuston and G. Stuart for critically reading the
manuscript, P. Andersen, B. Betz, J. Evans, K. Harris, E. v. Kitzing, R. Rahamimov
and K. Stratford for helpful discussions, and J. J. B. Jack for much-needed advice
and guidance to G.M. We thank K. Bauer, F. Helmchen, M. Huke, B. Manz and especially
A. Roth for computer programming, B. Werner for typing the manuscript, and M. Kaiser
for excellent technical assistance. Part of the project was supported by the Deutsche
Forschungsgemeinschaft (SFB-317)\r\nand the Wellcome Trust."
article_processing_charge: No
article_type: original
author:
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Guy
full_name: Major, Guy
last_name: Major
- first_name: Bert
full_name: Sakmann, Bert
last_name: Sakmann
citation:
ama: Jonas PM, Major G, Sakmann B. Quantal components of unitary EPSCs at the mossy
fibre synapse on CA3 pyramidal cells of rat hippocampus. Journal of Physiology.
1993;472:615-663. doi:10.1113/jphysiol.1993.sp019965
apa: Jonas, P. M., Major, G., & Sakmann, B. (1993). Quantal components of unitary
EPSCs at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus. Journal
of Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1993.sp019965
chicago: Jonas, Peter M, Guy Major, and Bert Sakmann. “Quantal Components of Unitary
EPSCs at the Mossy Fibre Synapse on CA3 Pyramidal Cells of Rat Hippocampus.” Journal
of Physiology. Wiley-Blackwell, 1993. https://doi.org/10.1113/jphysiol.1993.sp019965.
ieee: P. M. Jonas, G. Major, and B. Sakmann, “Quantal components of unitary EPSCs
at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus,” Journal
of Physiology, vol. 472. Wiley-Blackwell, pp. 615–663, 1993.
ista: Jonas PM, Major G, Sakmann B. 1993. Quantal components of unitary EPSCs at
the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus. Journal of
Physiology. 472, 615–663.
mla: Jonas, Peter M., et al. “Quantal Components of Unitary EPSCs at the Mossy Fibre
Synapse on CA3 Pyramidal Cells of Rat Hippocampus.” Journal of Physiology,
vol. 472, Wiley-Blackwell, 1993, pp. 615–63, doi:10.1113/jphysiol.1993.sp019965.
short: P.M. Jonas, G. Major, B. Sakmann, Journal of Physiology 472 (1993) 615–663.
date_created: 2018-12-11T12:03:31Z
date_published: 1993-12-01T00:00:00Z
date_updated: 2022-03-30T09:33:19Z
day: '01'
doi: 10.1113/jphysiol.1993.sp019965
extern: '1'
external_id:
pmid:
- '7908327'
intvolume: ' 472'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1160505
month: '12'
oa: 1
oa_version: Published Version
page: 615 - 663
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2913'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Quantal components of unitary EPSCs at the mossy fibre synapse on CA3 pyramidal
cells of rat hippocampus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 472
year: '1993'
...
---
_id: '3470'
abstract:
- lang: eng
text: Currents activated by glutamate receptor (GluR) agonists were recorded from
outside-out patches isolated from the soma of visually identified pyramidal neurones
of the (CA3 and CA1 region of rat hippocampal slices. α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic
acid (AMPA). L-glutamate (L-Glu), and kainate (KA) were delivered either by bath
application through perfusion of the recording chamber or by rapid application
via a piezo-driven two-barrelled fast application system. 2. Bath application
of each of the three agonists activated inward currents in all patches (n = 134)
at holding potentials of -50 or -60 mV. The current amplitude increased in size
between 3 to 30 μM-AMPA and 100 μM to 1 mM-KA. With this slow mode of bath application,
the responses showed no apparent desensitization even at saturating concentrations
of AMPA (30 μM) and KA (1 mM). 3. The ratio of currents activated by 30 μM-AMPA
and 300 μM-KA showed a characteristic difference between CA3 and CA1 neurones.
The ratio was 0.242 ± 0.028 (mean ± S.E.M., n = 16) for CA3 cell patches and 0.097
± 0.012 (n = 8) for CA1 cell patches indicating that GluRs in the two cell populations
are different. 4. The steady-state current-voltage relations (I-Vs) for AMPA-
and KA-activated currents showed pronounced outward rectification for both cell
types (when the main cations are Na+ in the bath and Cs+ in the pipette solution).
The current reversed close to 0 mV and the ratio of chord conductances 80 mV on
either side of the reversal potential was 2.66 for KA-activated currents in CA3
cell patches and 2.60 in CA1 cell patches. AMPA-activated currents showed a time-dependent
increase after steps to positive membrane potentials and a decrease after steps
to negative voltages, indicating that a gating process is responsible for outward
rectification of the steady-state I-IV. 5. The permeability (P) of GluR channels
was high for Na+ as compared to Cs+ for both cell types (P(Na)/P(Cs) = 0.88 and
0.84). The permeability was low for N-methyl-D-glucamine+ (P(NMG)/P(Cs) ≤ 0.03)
and Ca2+ (P(Ca)/P(Cs) ≤0.05). 6. The current noise level increased during application
of AMPA or KA. Apparent single-channel conductances obtained from fluctuation
analysis were higher for AMPA than for KA, but similar for both cell types. In
CA3 cell patches, AMPA activated channels with an apparent chord conductance of
7.2 pS, KA of 3.0 pS conductance. 7. Fast agonist application revealed desensitization
of GluR channels which was dependent on the type of agonist, currents activated
by AMPA and L-Glu rose rapidly to a peak and then desensitized to a steady-state
current. In contrast, currents activated by fast application of KA rose to a plateau
and did not desensitize. The steady state current expressed as a percentage of
the peak current was higher for L-Glu than for AMPA and slightly higher for CA3
than for CA1 cell patches. For CA3 cell patches, this fraction amounted to 6.2
%, with 300 μM-L-Glu and 2.8%, with 300 μM-AMPA. For CA1 cell patches, corresponding
values were 3.6 and 1.9 % 8. The dose response relations for the peak current
activated by AMPA and L-Glu and the steady-state current activated by KA were
similar for CA3 and CA1 cell patches. The order of potency was AMPA > L-Glu
≃ KA for both cell types EC50 values 189, 342 and 344 μM for CA3 cell patches
and 183, 424 and 474 μM for CA1 cell patches). In all cases, the Hill coefficients
ranged between 12 and 1.7. 8. The rise of AMPA and L-Glu-activated currents became
faster with increasing agonist concentration for both cell types. With L-Glu,
rise times decreased from about 3 ms at 100 μM to 500 μs at 3 mM. The delay for
agonist concentrations ≥ 300 μM was described by the sum of two exponential functions.
The time constant of the predominant fast component was slightly concentration
dependent and decreased from about 12 ms at 300 μM to 8 ms at 3 mM-L-Glu. 10.
The current voltage relations of the peak currents activated by 300 μM-AMPA were
linear for both cell types with a reversal potential close to OmV. 11. It is concluded
that the GluR channels in pyramidal cells of hippocampal CA3 and CA1 regions are
distinet but share many pharmacological and functional properties. Comparison
of the properties of native and recombinant GluRs suggests that in both CA3 and
CA1 regions GluR channels are hetero-oligomers containing the GluR-B subunit.
acknowledgement: "We thank Dr D. Colquhoun, Dr J. P. Ruppersberg and Dr T. A. Verdoorn
for critically reading the manuscript, K. Bauer, C. Busch and F. Helmchen for computer
programming, and M. Kaiser for technical assistance. \r\n"
article_processing_charge: No
article_type: original
author:
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Bert
full_name: Sakmann, Bert
last_name: Sakmann
citation:
ama: Jonas PM, Sakmann B. Glutamate receptor channels in isolated patches from CA1
and CA3 pyramidal cells of rat hippocampal slices. Journal of Physiology.
1992;455:143-171. doi:10.1113/jphysiol.1992.sp019294
apa: Jonas, P. M., & Sakmann, B. (1992). Glutamate receptor channels in isolated
patches from CA1 and CA3 pyramidal cells of rat hippocampal slices. Journal
of Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1992.sp019294
chicago: Jonas, Peter M, and Bert Sakmann. “Glutamate Receptor Channels in Isolated
Patches from CA1 and CA3 Pyramidal Cells of Rat Hippocampal Slices.” Journal
of Physiology. Wiley-Blackwell, 1992. https://doi.org/10.1113/jphysiol.1992.sp019294 .
ieee: P. M. Jonas and B. Sakmann, “Glutamate receptor channels in isolated patches
from CA1 and CA3 pyramidal cells of rat hippocampal slices,” Journal of Physiology,
vol. 455. Wiley-Blackwell, pp. 143–171, 1992.
ista: Jonas PM, Sakmann B. 1992. Glutamate receptor channels in isolated patches
from CA1 and CA3 pyramidal cells of rat hippocampal slices. Journal of Physiology.
455, 143–171.
mla: Jonas, Peter M., and Bert Sakmann. “Glutamate Receptor Channels in Isolated
Patches from CA1 and CA3 Pyramidal Cells of Rat Hippocampal Slices.” Journal
of Physiology, vol. 455, Wiley-Blackwell, 1992, pp. 143–71, doi:10.1113/jphysiol.1992.sp019294 .
short: P.M. Jonas, B. Sakmann, Journal of Physiology 455 (1992) 143–171.
date_created: 2018-12-11T12:03:30Z
date_published: 1992-09-01T00:00:00Z
date_updated: 2022-03-16T13:01:55Z
day: '01'
doi: '10.1113/jphysiol.1992.sp019294 '
extern: '1'
external_id:
pmid:
- '1282929 '
intvolume: ' 455'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.1992.sp019294
month: '09'
oa: 1
oa_version: Published Version
page: 143 - 171
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2917'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Glutamate receptor channels in isolated patches from CA1 and CA3 pyramidal
cells of rat hippocampal slices
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 455
year: '1992'
...
---
_id: '3471'
abstract:
- lang: eng
text: 1. Outside-out patches were isolated from granule cells of dentate gyrus and
pyramidal cells of CA3 and CA1 regions of rat hippocampal slices. Patches were
exposed briefly to L-glutamate using a piezo-driven double-barrelled application
pipette. 2. Applications of glutamate (1 mM) of 1 ms duration activated patch
currents which rose and decayed rapidly. The 20-80% rise time of these glutamate
receptor (GluR)-mediated currents was usually 0.2-0.6 ms. At -50 mV the peak current
varied from 10 to 500 pA in different patches. 3. The peak current-voltage relation
for brief pulses of 1 mM glutamate was virtually linear in normal extracellular
solution for patches from the three cell types (-100 to 60 mV). 4. The permeability
of GluR channels activated at the peak to Ca2+, relative to K+, was less than
0.1 for all three cell types (under bi-ionic conditions with Ca2+ on the extracellular
side and K+ on the intracellular side of the membrane). 5. The offset decay time
constant of the current following 1 ms pulses of 1 mM glutamate was brief, with
mean values of 3.0 +/- 0.8, 2.5 +/- 0.7, and 2.3 +/- 0.7 ms for dentate, CA3 and
CA1 cell patches, respectively. Offset time constants were independent of membrane
potential and independent of glutamate concentration (200 microM and 1 mM) for
the three cell types. 6. Applications of 1 mM glutamate of 100 ms duration showed
that glutamate responses desensitized rapidly. The time constants for desensitization
were 9.4 +/- 2.7, 11.3 +/- 2.8, and 9.3 +/- 2.8 ms for patches from dentate, CA3
and CA1 cells respectively. Desensitization time constants were only weakly dependent
on glutamate concentration (200 microM and 1 mM) for the three cell types. Thus
offset time constants are about four times faster than desensitization time constants
for both glutamate concentrations. 7. Double pulse application of glutamate indicated
that even a 1 ms pulse of 1 mM glutamate causes partial (about 60%) desensitization
of GluR channels. The time course of recovery from desensitization was slower
in dentate gyrus granule cell patches than in CA3 or CA1 pyramidal cell patches.
8. Desensitization was studied at equilibrium by exposing patches to low glutamate
concentrations for at least 15 s before a 1 ms test pulse of 1 mM glutamate.
acknowledgement: 'We thank Drs N.Burnashev, P. Ruppersberg , and G.Stuart for critically
reading the manuscript, and Marlies Kaiser for technical assistance. D.C.is a recipient
of a Humboldt prize. '
article_processing_charge: No
article_type: original
author:
- first_name: D.
full_name: Colquhoun, D.
last_name: Colquhoun
- 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: Bert
full_name: Sakmann, Bert
last_name: Sakmann
citation:
ama: Colquhoun D, Jonas PM, Sakmann B. Action of brief pulses of glutamate on AMPA/kainate
receptors in patches from different neurones of rat hippocampal slices. Journal
of Physiology. 1992;458:261-287. doi:10.1113/jphysiol.1992.sp019417
apa: Colquhoun, D., Jonas, P. M., & Sakmann, B. (1992). Action of brief pulses
of glutamate on AMPA/kainate receptors in patches from different neurones of rat
hippocampal slices. Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.1992.sp019417
chicago: Colquhoun, D., Peter M Jonas, and Bert Sakmann. “Action of Brief Pulses
of Glutamate on AMPA/Kainate Receptors in Patches from Different Neurones of Rat
Hippocampal Slices.” Journal of Physiology. Wiley-Blackwell, 1992. https://doi.org/10.1113/jphysiol.1992.sp019417.
ieee: D. Colquhoun, P. M. Jonas, and B. Sakmann, “Action of brief pulses of glutamate
on AMPA/kainate receptors in patches from different neurones of rat hippocampal
slices,” Journal of Physiology, vol. 458. Wiley-Blackwell, pp. 261–287,
1992.
ista: Colquhoun D, Jonas PM, Sakmann B. 1992. Action of brief pulses of glutamate
on AMPA/kainate receptors in patches from different neurones of rat hippocampal
slices. Journal of Physiology. 458, 261–287.
mla: Colquhoun, D., et al. “Action of Brief Pulses of Glutamate on AMPA/Kainate
Receptors in Patches from Different Neurones of Rat Hippocampal Slices.” Journal
of Physiology, vol. 458, Wiley-Blackwell, 1992, pp. 261–87, doi:10.1113/jphysiol.1992.sp019417.
short: D. Colquhoun, P.M. Jonas, B. Sakmann, Journal of Physiology 458 (1992) 261–287.
date_created: 2018-12-11T12:03:30Z
date_published: 1992-12-01T00:00:00Z
date_updated: 2022-03-16T12:41:01Z
day: '01'
doi: 10.1113/jphysiol.1992.sp019417
extern: '1'
external_id:
pmid:
- '1338788'
intvolume: ' 458'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1175155/
month: '12'
oa: 1
oa_version: Published Version
page: 261 - 287
pmid: 1
publication: Journal of Physiology
publication_identifier:
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2916'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Action of brief pulses of glutamate on AMPA/kainate receptors in patches from
different neurones of rat hippocampal slices
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 458
year: '1992'
...
---
_id: '3467'
abstract:
- lang: eng
text: The effects of mast cell degranulating peptide (MCDP), a toxin from the honey
bee, and of dendrotoxin (DTX), a toxin from the green mamba snake, were studied
in voltage-clamped experiments with myelinated nerve fibres of Xenopus. MCDP and
DTX blocked part of the K+ current. About 20% of the K+ current, however, was
resistant to the toxins even in high concentrations. In Ringer solution half-maximal
block was reached with concentrations of 33 nM MCDP and 11 nM DTX. In high-K+
solution the potency of both toxins was lower. β-Bungarotoxin (β-BuTX), another
snake toxin, also blocked part of the K+ current, but was less potent than MCDP
and DTX. Tail currents in high-K+ solution were analysed and three K+ current
components were separated according to Dubois (1981b). Both MCDP and DTX selectively
blocked a fast deactivating, slowly inactivating K+ current component which steeply
activates between E = -60 mV and E = -40 mV (component f1). In concentrations
around 100 nM, MCDP and DTX blocked neither the slow K+ current (component s)
nor the fast deactivating, rapidly inactivating K+ current which activates between
E = -40 mV and E = 20 mV (component f2). Similar results could be derived from
K+ outward currents in Ringer solution. In high-K+, IC50 of MCDP for component
f1 was 99 nM, whereas it was 7.6 μM for f2. Corresponding values for DTX are 68
nM and 1.8 μM. Binding studies with nerve fibre membranes of Xenopus reveal high-affinity
binding sites for 125I-labelled DTX )K(D) = 22 pM in Ringer solution and 81 pM
in high-K+ solution). 125I-labelled DTX can be displaced from its sites completely
by unlabelled DTX, toxin I (black mamba toxin), MCDP, and partially by β-BuTX.
Immunocytochemical staining demonstrates that binding sites for DTX are present
in nodal and paranodal regions of the axonal membrane. The axonal membrane of
motor and sensory nerve fibres is equipped with three types of well-characterized
K+ channels and constitutes so far the best preparation to study MCDP- and DTX-sensitive
K+ channels with electrophysiological and biochemical methods.
acknowledgement: "We thank Professor E. Habermann for critical reading of the manuscript
and E. Schmidt and J. Schafer for technical assistance. Financial support by the
Deutsche Forschungsgemeinschaft (Vo 188/13-1 and SFB 249) is gratefully acknowledged.\r\n"
article_processing_charge: No
article_type: original
author:
- first_name: Michael
full_name: Bräu, Michael
last_name: Bräu
- first_name: Florian
full_name: Dreyer, Florian
last_name: Dreyer
- 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: Holger
full_name: Repp, Holger
last_name: Repp
- first_name: Werner
full_name: Vogel, Werner
last_name: Vogel
citation:
ama: 'Bräu M, Dreyer F, Jonas PM, Repp H, Vogel W. A K+ channel in Xenopus nerve
fibres selectively blocked by bee and snake toxins: binding and voltage-clamp
experiments. Journal of Physiology. 1990;420:365-385. doi:10.1113/jphysiol.1990.sp017918'
apa: 'Bräu, M., Dreyer, F., Jonas, P. M., Repp, H., & Vogel, W. (1990). A K+
channel in Xenopus nerve fibres selectively blocked by bee and snake toxins: binding
and voltage-clamp experiments. Journal of Physiology. Wiley-Blackwell.
https://doi.org/10.1113/jphysiol.1990.sp017918'
chicago: 'Bräu, Michael, Florian Dreyer, Peter M Jonas, Holger Repp, and Werner
Vogel. “A K+ Channel in Xenopus Nerve Fibres Selectively Blocked by Bee and Snake
Toxins: Binding and Voltage-Clamp Experiments.” Journal of Physiology.
Wiley-Blackwell, 1990. https://doi.org/10.1113/jphysiol.1990.sp017918.'
ieee: 'M. Bräu, F. Dreyer, P. M. Jonas, H. Repp, and W. Vogel, “A K+ channel in
Xenopus nerve fibres selectively blocked by bee and snake toxins: binding and
voltage-clamp experiments,” Journal of Physiology, vol. 420. Wiley-Blackwell,
pp. 365–385, 1990.'
ista: 'Bräu M, Dreyer F, Jonas PM, Repp H, Vogel W. 1990. A K+ channel in Xenopus
nerve fibres selectively blocked by bee and snake toxins: binding and voltage-clamp
experiments. Journal of Physiology. 420, 365–385.'
mla: 'Bräu, Michael, et al. “A K+ Channel in Xenopus Nerve Fibres Selectively Blocked
by Bee and Snake Toxins: Binding and Voltage-Clamp Experiments.” Journal of
Physiology, vol. 420, Wiley-Blackwell, 1990, pp. 365–85, doi:10.1113/jphysiol.1990.sp017918.'
short: M. Bräu, F. Dreyer, P.M. Jonas, H. Repp, W. Vogel, Journal of Physiology
420 (1990) 365–385.
date_created: 2018-12-11T12:03:29Z
date_published: 1990-01-01T00:00:00Z
date_updated: 2022-02-23T16:10:03Z
day: '01'
doi: 10.1113/jphysiol.1990.sp017918
extern: '1'
external_id:
pmid:
- '2324990'
intvolume: ' 420'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1190055/
month: '01'
oa: 1
oa_version: None
page: 365 - 385
pmid: 1
publication: Journal of Physiology
publication_identifier:
eissn:
- 1469-7793
issn:
- 0022-3751
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2920'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'A K+ channel in Xenopus nerve fibres selectively blocked by bee and snake
toxins: binding and voltage-clamp experiments'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 420
year: '1990'
...