Neuroscience Graduate Program, Oregon Health & Science University, Portland, OR 97239, USA; Vollum Institute & Oregon Hearing Research Center, Oregon Health & Science University, Portland, OR 97239, USA.
Vollum Institute & Oregon Hearing Research Center, Oregon Health & Science University, Portland, OR 97239, USA.
Neuron. 2014 Jul 16;83(2):324-330. doi: 10.1016/j.neuron.2014.06.008. Epub 2014 Jul 4.
Voltage-gated ion channels amplify, compartmentalize, and normalize synaptic signals received by neurons. We show that voltage-gated channels activated during subthreshold glutamatergic synaptic potentials in a principal cell generate an excitatory→inhibitory synaptic sequence that excites electrically coupled interneurons. In fusiform cells of the dorsal cochlear nucleus, excitatory synapses activate a TTX-sensitive Na(+) conductance and deactivate a resting Ih conductance, leading to a striking reshaping of the synaptic potential. Subthreshold voltage changes resulting from activation/deactivation of these channels subsequently propagate through gap junctions, causing slow excitation followed by inhibition in GABAergic stellate interneurons. Gap-junction-mediated transmission of voltage-gated signals accounts for the majority of glutamatergic signaling to interneurons, such that subthreshold synaptic events from a single principal cell are sufficient to drive spikes in coupled interneurons. Thus, the interaction between a principal cell's synaptic and voltage-gated channels may determine the spike activity of networks without firing a single action potential.
电压门控离子通道可放大、分隔和规范神经元接收的突触信号。我们表明，在主细胞中受阈下谷氨酸能突触电位激活的电压门控通道会产生兴奋性→抑制性突触序列，从而兴奋电耦联的中间神经元。在耳蜗背核的梭形细胞中，兴奋性突触会激活一种 TTX 敏感的 Na(+)电导，并失活静息 Ih 电导，从而导致突触电位的明显重塑。这些通道的激活/失活所产生的阈下电压变化随后通过缝隙连接传播，导致 GABA 能星状中间神经元的缓慢兴奋继之以抑制。电压门控信号的缝隙连接介导传递解释了大多数谷氨酸能信号向中间神经元的传递，因此，单个主细胞的阈下突触事件足以驱动偶联中间神经元的尖峰。因此，主细胞的突触和电压门控通道之间的相互作用可能决定了网络的尖峰活动，而无需触发单个动作电位。
