Umemiya M, Berger A J
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.
Neuron. 1994 Dec;13(6):1439-46. doi: 10.1016/0896-6273(94)90429-4.
Multiple types of calcium channels are responsible for calcium influx that triggers transmitter release in the mammalian CNS. To test the contribution of each calcium channel type on synaptic modulation, we recorded calcium currents from somata of presynaptic interneurons and unitary glycinergic postsynaptic currents in the rat brainstem. In interneuron somata, A1 receptor activation inhibited predominantly N-type (omega-conotoxin GVIA-sensitive) and, to a lesser extent, P-type (omega-agatoxin IVA-sensitive) channels. At the presynaptic terminal, N- and P-type channels mediated synaptic transmission. omega-CgTx occluded synaptic inhibition by A1 receptor activation, suggesting that synaptic inhibition was mediated predominantly by N-type channel inhibition. A2 receptor activation facilitated synaptic transmission, probably through potentiation of P-type channels at the presynaptic terminal.
多种类型的钙通道负责钙内流，而钙内流会触发哺乳动物中枢神经系统中的递质释放。为了测试每种钙通道类型对突触调制的作用，我们记录了大鼠脑干中突触前中间神经元胞体的钙电流以及单一甘氨酸能突触后电流。在中间神经元胞体中，A1受体激活主要抑制N型（对ω-芋螺毒素GVIA敏感）通道，在较小程度上抑制P型（对ω-阿加毒素IVA敏感）通道。在突触前终末，N型和P型通道介导突触传递。ω-芋螺毒素阻断了A1受体激活引起的突触抑制，这表明突触抑制主要是由N型通道抑制介导的。A2受体激活促进了突触传递，可能是通过增强突触前终末的P型通道实现的。
