MECHANISMS UNDERLYING THE ENHANCEMENT OF EXCITATORY SYNAPTIC TRANSMISSION IN BASOLATERAL AMYGDALA NEURONS OF THE KINDLING RAT

Citation
Y. Shoji et al., MECHANISMS UNDERLYING THE ENHANCEMENT OF EXCITATORY SYNAPTIC TRANSMISSION IN BASOLATERAL AMYGDALA NEURONS OF THE KINDLING RAT, Journal of neurophysiology, 80(2), 1998, pp. 638-646
Citations number
64
Categorie Soggetti
Neurosciences,Physiology
Journal title
ISSN journal
00223077
Volume
80
Issue
2
Year of publication
1998
Pages
638 - 646
Database
ISI
SICI code
0022-3077(1998)80:2<638:MUTEOE>2.0.ZU;2-V
Abstract
To elucidate the mechanism underlying epileptiform discharges in kindl ed rats, synaptic responses in kindled basolateral amygdala neurons in vine were compared with those from control rats by using intracellula r and whole cell patch-clamp recordings. In kindled neurons, electrica l stimulation of the stria terminalis induced epileptiform discharges. The resting potential, apparent input resistance, current-voltage rel ationship of the membrane, and the threshold, amplitude, and duration of action potentials in kindled neurons were not different from those in control neurons. The electrical stimulation of stria terminalis eli cited excitatory postsynaptic potentials (EPSPs) and DL-2-amino-5-phos phonopentanoic acid(AP5)-sensitive and 6-cyano-7-nitroquinoxaline-2,3- dione (CNQX)-sensitive excitatory postsynaptic currents (EPSCs). The a mplitude of evoked EPSPs and of evoked APS-sensitive and CNQX-sensitiv e EPSCs were enhanced markedly, whereas fast and slow inhibitory posts ynaptic potentials (IPSPs) induced by electrical stimulation of latera l amygdaloid nucleus were not significantly different. The rise time a nd the decay time constant of the evoked CNQX-sensitive EPSCs were sho rtened, whereas the rise time of the evoked AP5-sensitive EPSCs was sh ortened, but the decay time constants were not significantly different . In both tetrodotoxin (TTX)-containing me dium and low Ca2+ and TTX-c ontaining medium, the frequency and amplitude of spontaneous EPSCs wer e increased in kindled neurons. These increases are presumably due to nearly synchronous multiquantal events resulted from the increased pro bability of Glu release at the nerve terminals. The rise time of evoke d CNQX- and AP5-sensitive EPSCs and the decay time constant of evoked CNQX-sensitive EPSCs were shortened, suggesting that excitatory synaps es at the proximal dendrite and/or the soma in kindled neurons may con tribute more effectively to generate evoked EPSCs than those at distal dendrites. In conclusion, the increases in the amplitudes of spontane ous and evoked EPSCs and in the frequency of spontaneous EPSCs may con tribute to the epileptiform discharges in kindled neurons.