Satake Shin'Ichiro, Inoue Tsuyoshi, Imoto Keiji
Department of Information Physiology, National Institute for Physiological Sciences (NIPS), 5-1 Higashiyama, Myodaiji-cho, Okazaki, 444-8787, Japan.
School of Life Science, The Graduate University for Advanced Studies (SOKENDAI), 5-1 Higashiyama, Myodaiji-cho, Okazaki, 444-8787, Japan.
Cerebellum. 2016 Apr;15(2):201-7. doi: 10.1007/s12311-015-0677-5.
The number of synaptic vesicles released during fast release plays a major role in determining the strength of postsynaptic response. However, it remains unresolved how the number of vesicles released in response to action potentials is controlled at a single synapse. Recent findings suggest that the Cav2.1 subtype (P/Q-type) of voltage-gated calcium channels is responsible for inducing presynaptic multivesicular release (MVR) at rat cerebellar glutamatergic synapses from granule cells to molecular layer interneurons. The topographical distance from Cav2.1 channels to exocytotic Ca(2+) sensors is a critical determinant of MVR. In physiological trains of presynaptic neurons, MVR significantly impacts the excitability of postsynaptic neurons, not only by increasing peak amplitude but also by prolonging decay time of the postsynaptic currents. Therefore, MVR contributes additional complexity to neural encoding and processing in the cerebellar cortex.
快速释放过程中释放的突触小泡数量在决定突触后反应强度方面起主要作用。然而,在单个突触处,动作电位引发的小泡释放数量是如何受到控制的,这一问题仍未得到解决。最近的研究结果表明,电压门控钙通道的Cav2.1亚型(P/Q型)负责在大鼠小脑颗粒细胞到分子层中间神经元的谷氨酸能突触处诱导突触前多泡释放(MVR)。从Cav2.1通道到胞吐Ca(2+)传感器的拓扑距离是MVR的关键决定因素。在突触前神经元的生理序列中,MVR不仅通过增加峰值幅度,还通过延长突触后电流的衰减时间,显著影响突触后神经元的兴奋性。因此,MVR为小脑皮质的神经编码和处理增添了额外的复杂性。