Calton J L, Kang M H, Wilson W A, Moore S D
Department of Psychiatry, Durham, North Carolina 27705, USA.
J Neurophysiol. 2000 Feb;83(2):685-92. doi: 10.1152/jn.2000.83.2.685.
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.
在全细胞电流钳记录过程中，杏仁核基底外侧区锥体细胞的传入刺激产生了由N-甲基-D-天冬氨酸（NMDA）和非NMDA谷氨酸受体介导的混合兴奋性突触后电位（EPSP）。在存在GABA(A)受体阻断的情况下，混合EPSP引发了一个大的“全或无”去极化事件。这个引发的事件是电压依赖性的，并且有一个明显的激活阈值。在河豚毒素（TTX）存在的情况下，外源性谷氨酸引发的类似现象被镉离子（Cd(2+)）阻断，这表明该事件是一个钙离子峰电位。选择性谷氨酸能阻断显示，这些钙离子峰电位很容易被引发NMDA EPSP的单个传入刺激脉冲所募集。相比之下，即使在最大刺激强度下，单个刺激诱导产生的非NMDA EPSP也未能引发钙离子峰电位，尽管这些非NMDA EPSP比混合EPSP更有效地使胞体去极化。用环噻嗪延长非NMDA EPSP或短暂的刺激串也无法引发钙离子峰电位。用细胞内铯离子（Cs(+)）阻断钾离子通道能使单个非NMDA EPSP激活钙离子峰电位。电压依赖性钙通道优先被NMDA受体介导 的EPSP激活这一发现，为不依赖于通过NMDA受体的钙离子内流的NMDA受体依赖性可塑性提供了一种机制。
