| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
The Journal of Neurophysiology Vol. 87 No. 2 February 2002, pp. 925-936
Copyright ©2002 by the American Physiological Society
Department of Psychiatry and Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110
He, Yejun,
Charles F. Zorumski, and
Steven Mennerick.
Contribution of Presynaptic Na+ Channel
Inactivation to Paired-Pulse Synaptic Depression in Cultured
Hippocampal Neurons. J. Neurophysiol. 87: 925-936, 2002. Paired-pulse depression (PPD)
of synaptic transmission is important for neuronal information
processing. Historically, depletion of the readily releasable pool of
synaptic vesicles has been proposed as the major component of PPD.
Recent results suggest, however, that other mechanisms may be involved
in PPD, including inactivation of presynaptic voltage-dependent sodium
channels (NaChs), which may influence coupling of action potentials to
transmitter release. In hippocampal cultures, we have examined the
potential role and relative contribution of presynaptic NaCh
inactivation in excitatory postsynaptic current (EPSC) PPD. Based on
current- and voltage-clamp recordings from somas, our data suggest that
NaCh inactivation could potentially participate in PPD. Paired
stimulation of somatic action potentials (20- to 100-ms interval)
results in subtle changes in action potential shape that are mimicked
by low concentrations of tetrodotoxin (TTX) and that appear to be
generated by a combination of fast and slow recovery from NaCh
inactivation. Dilute concentrations of TTX dramatically depress
glutamate release. However, we find evidence for only minimal
contribution of NaCh inactivation to EPSC PPD under basal conditions.
Hyperpolarization of presynaptic elements to speed recovery from
inactivation or increasing the driving force on
Na+ ions through active NaChs had minimal effects
on PPD while more robustly reversing the effects of pharmacological
NaCh blockade. On the other hand, slight depolarization of the
presynaptic membrane potential, by elevating extracellular
[K+]o, significantly
increased PPD and frequency-dependent depression of EPSCs during short
trains of action potentials. The results suggest that NaCh inactivation
is poised to modulate EPSC amplitude with small tonic depolarizations
that likely occur with physiological or pathophysiological activity.
This article has been cited by other articles:
|
|
 |
|
  C. F. Stevens and J. H. Williams Discharge of the Readily Releasable Pool With Action Potentials at Hippocampal Synapses J Neurophysiol, December 1, 2007; 98(6): 3221 - 3229. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. L. Moulder and S. Mennerick Synaptic Vesicles: Turning Reluctance Into Action Neuroscientist, February 1, 2006; 12(1): 11 - 15. [Abstract] [PDF]
|
|
|
|
 |
|
 R. M. Leao, C. Kushmerick, R. Pinaud, R. Renden, G.-L. Li, H. Taschenberger, G. Spirou, S. R. Levinson, and H. von Gersdorff Presynaptic Na+ Channels: Locus, Development, and Recovery from Inactivation at a High-Fidelity Synapse J. Neurosci., April 6, 2005; 25(14): 3724 - 3738. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Munoz-Cuevas, H. Vara, and A. Colino Characterization of release-independent short-term depression in the juvenile rat hippocampus J. Physiol., July 15, 2004; 558(2): 527 - 548. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Otsu, V. Shahrezaei, B. Li, L. A. Raymond, K. R. Delaney, and T. H. Murphy Competition between Phasic and Asynchronous Release for Recovered Synaptic Vesicles at Developing Hippocampal Autaptic Synapses J. Neurosci., January 14, 2004; 24(2): 420 - 433. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P. Meeks and S. Mennerick Selective Effects of Potassium Elevations on Glutamate Signaling and Action Potential Conduction in Hippocampus J. Neurosci., January 7, 2004; 24(1): 197 - 206. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Daoudal and D. Debanne Long-Term Plasticity of Intrinsic Excitability: Learning Rules and Mechanisms Learn. Mem., November 1, 2003; 10(6): 456 - 465. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Nunez, E. Carro, and I. Torres-Aleman Insulin-Like Growth Factor I Modifies Electrophysiological Properties of Rat Brain Stem Neurons J Neurophysiol, June 1, 2003; 89(6): 3008 - 3017. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Debanne and M. Russier Axonal propagation: does the spike stop here? J. Physiol., May 1, 2003; 548(3): 663 - 663. [Full Text] [PDF]
|
|
|
|
|
|
M. Raastad and G. M G Shepherd Single-axon action potentials in the rat hippocampal cortex J. Physiol., May 1, 2003; 548(3): 745 - 752. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Saviane, L. P Savtchenko, G. Raffaelli, L. L Voronin, and E. Cherubini Frequency-dependent shift from paired-pulse facilitation to paired-pulse depression at unitary CA3-CA3 synapses in the rat hippocampus J. Physiol., October 15, 2002; 544(2): 469 - 476. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kirischuk, J. D Clements, and R. Grantyn Presynaptic and postsynaptic mechanisms underlie paired pulse depression at single GABAergic boutons in rat collicular cultures J. Physiol., August 15, 2002; 543(1): 99 - 116. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. H L Chan, C. S-Y Lin, E. Pierrot-Deseilligny, and D. Burke Excitability changes in human peripheral nerve axons in a paradigm mimicking paired-pulse transcranial magnetic stimulation J. Physiol., August 1, 2002; 542(3): 951 - 961. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
