JN Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Neurophysiol 56: 1424-1438, 1986;
0022-3077/86 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gardner, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gardner, D.

Journal of Neurophysiology, Vol 56, Issue 5 1424-1438, Copyright © 1986 by APS


ARTICLES

Variations in amplitude and time course of inhibitory postsynaptic currents

D. Gardner

In order to examine the relative contributions of changes in amplitude and time course to synaptic plasticity, variations in peak amplitude and time constant of decay have been analyzed from inhibitory postsynaptic currents (PSC) recorded in voltage-clamped Aplysia buccal ganglia neurons. In these cells, synaptic currents with single time constant decay can be recorded with low noise under well-controlled space clamp. Over a population of 36 neurons, duration was more narrowly distributed than amplitude, but each varied. The coefficient of variation (CV) was 0.21 for decay time constant (tau) and 0.87 for peak conductance (g peak). Population variances are larger than can be accounted for by such variables as temperature and noise amplitude, suggesting that functional modifications alter each of these determinants of synaptic effectiveness over the long term. Recordings of up to several hundred PSC in each of 16 neurons show that both PSC amplitude and time course recorded in a single cell can vary independently over short time spans. Decay remained single exponential as time course changed. CV for tau averaged 0.11; CV for g peak was 0.19. Variability of tau was not an artifact of amplitude; CV was relatively uncorrelated with current amplitudes or sample size. Smoothing and adding excess noise to each individual PSC of a set produced only small changes to CV, showing that variability was not an artifact of noise. Several specific manipulations of the presynaptic neuron altered both PSC amplitude and time course. Tetanic stimulation of the presynaptic neuron produced short-term potentiation of both amplitude and time course of subsequent PSCs. Peak amplitude was increased by 80%; tau by 12%. Reducing interspike intervals from 10 to 1 s produced habituation of both amplitude and time course, with g peak decreasing by 35 to 40% and tau by 10%. Conditioning DC depolarization of the presynaptic neuron enhanced PSC amplitude with little effect on decay time constant. Although short-term plastic changes affect PSC amplitude more than duration, each is alterable. Parallel changes in both can synergistically alter synaptic charge transfer, and therefore efficacy. Similar mechanisms may produce larger long-term differences seen between neurons.


This article has been cited by other articles:


Home page
J. Neurophysiol.Home page
C. G. Evans, A. Romero, and E. C. Cropper
Inhibition of Afferent Transmission in the Feeding Circuitry of Aplysia: Persistence Can Be as Important as Size
J Neurophysiol, May 1, 2005; 93(5): 2940 - 2949.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online