Enhancement Of Synaptic Excitation By GABAA Receptor-Antagonists In Rat
Embryonic Midbrain Culture.
JUTTA ROHRBACHER, KATJA SAUER, ANDREA LEWEN, AND ULRICH MISGELD.
I. Physiologisches Institut der Universit„t Heidelberg, Im Neuenheimer Feld
326, D-69120 Heidelberg, Germany.
APStracts 4:298N, 1997.
ABSTRACT
Alterations of synaptic excitation induced by exposure to [gamma]-aminobutyric
acid-A (GABAA) receptor-antagonists were investigated employing tight seal
whole cell recording from single neurons or pairs of neurons in rat embryonic
midbrain culture. Application of GABAA receptor-antagonists led to sustained
depolarizations followed by synchronous paroxysmal depolarization shifts
(PDSs). PDSs induced a transient increase in miniature excitatory postsynaptic
currents in the presence as well as in the absence of a N-methyl-D-aspartate
receptor-antagonist. The increase in glutamate release supports the excitatory
drive required to re-initiate PDSs from the quiescent interburst intervals.
After washout of GABAA receptor-antagonists, synaptic activity remained
grouped, regardless of the presence or absence of PDS blockade by tetrodotoxin
(TTX). Impediment of action potential-triggered transmitter release by Cd2+ or
TTX also induced grouped activity. We conclude that changes in synaptic
excitation are produced by the impaired GABAA inhibition per se and by the
initiation of PDSs.
Received 2 September 1997; accepted in final form 22 October 1997.
APS Manuscript Number J719-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 29 October 1997