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J Neurophysiol 83: 685-692, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 83 No. 2 February 2000, pp. 685-692
Copyright ©2000 by the American Physiological Society

NMDA-Receptor-Dependent Synaptic Activation of Voltage-Dependent Calcium Channels in Basolateral Amygdala

Jeffrey L. Calton,3 Maeng-Hee Kang,4 Wilkie A. Wilson,2,4 and Scott D. Moore1,3

Divisions of  1Psychiatry and  2Neurology Research, Durham Veterans Administration Medical Center, and Departments of  3Psychiatry and  4Pharmacology, Duke University Medical Center, Durham, North Carolina 27705

Calton, Jeffrey L., Maeng-Hee Kang, Wilkie A. Wilson, and Scott D. Moore. NMDA-Receptor-Dependent Synaptic Activation of Voltage-Dependent Calcium Channels in Basolateral Amygdala. J. Neurophysiol. 83: 685-692, 2000. Afferent stimulation of pyramidal cells in the basolateral amygdala produced mixed excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors during whole cell current-clamp recordings. In the presence of GABAA receptor blockade, the mixed EPSPs recruited a large "all-or-none" depolarizing event. This recruited event was voltage dependent and had a distinct activation threshold. An analogous phenomenon elicited by exogenous glutamate in the presence of tetrodotoxin (TTX) was blocked by Cd2+, suggesting that the event was a Ca2+ spike. Selective glutamatergic blockade revealed that these Ca2+ spikes were recruited readily by single afferent stimulus pulses that elicited NMDA EPSPs. In contrast, non-NMDA EPSPs induced by single stimuli failed to elicit the Ca2+ spike even at maximal stimulus intensities although these non-NMDA EPSPs depolarized the soma more effectively than mixed EPSPs. Elongation of non-NMDA EPSPs by cyclothiazide or brief trains of stimulation were also unable to elicit the Ca2+ spike. Blockade of K+ channels with intracellular Cs+ enabled single non-NMDA EPSPs to activate the Ca2+ spike. The finding that voltage-dependent calcium channels are activated preferentially by NMDA-receptor-mediated EPSPs provides a mechanism for NMDA-receptor-dependent plasticity independent of Ca2+ influx through the NMDA receptor.




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