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
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.