NMDA-Receptor-dependent synaptic activation of voltage-dependent calcium channels in basolateral amygdala. Export

@article{citeulike:2307823, abstract = {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 GABA(A) 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 Cd(2+), suggesting that the event was a Ca(2+) spike. Selective glutamatergic blockade revealed that these Ca(2+) 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 Ca(2+) 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 Ca(2+) spike. Blockade of K(+) channels with intracellular Cs(+) enabled single non-NMDA EPSPs to activate the Ca(2+) 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 Ca(2+) influx through the NMDA receptor.}, address = {Department of Psychiatry, Durham, North Carolina 27705, USA.}, author = {Calton, J. L. and Kang, M. H. and Wilson, W. A. and Moore, S. D.}, citeulike-article-id = {2307823}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/10669484}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=10669484}, issn = {0022-3077}, journal = {J Neurophysiol}, keywords = {bla, caesium, nmdar}, month = {February}, number = {2}, pages = {685--692}, posted-at = {2008-01-30 16:06:50}, priority = {2}, title = {NMDA-Receptor-dependent synaptic activation of voltage-dependent calcium channels in basolateral amygdala.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/10669484}, volume = {83}, year = {2000} }

TY - JOUR ID - citeulike:2307823 L3 - citeulike-article-id:2307823 N2 - 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 GABA(A) 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 Cd(2+), suggesting that the event was a Ca(2+) spike. Selective glutamatergic blockade revealed that these Ca(2+) 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 Ca(2+) 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 Ca(2+) spike. Blockade of K(+) channels with intracellular Cs(+) enabled single non-NMDA EPSPs to activate the Ca(2+) 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 Ca(2+) influx through the NMDA receptor. IS - 2 JF - J Neurophysiol SN - 0022-3077 AD - Department of Psychiatry, Durham, North Carolina 27705, USA. EP - 692 TI - NMDA-Receptor-dependent synaptic activation of voltage-dependent calcium channels in basolateral amygdala. VL - 83 SP - 685 KW - bla KW - caesium KW - nmdar AU - Calton, JL AU - Kang, MH AU - Wilson, WA AU - Moore, SD PY - 2000/02// UR - http://view.ncbi.nlm.nih.gov/pubmed/10669484 ER -