基底神经节中γ-氨基丁酸（GABA）释放的突触前调制

Presynaptic modulation of GABA release in the basal ganglia.

作者信息

Misgeld Ulrich, Drew Geoffrey, Yanovsky Yevgenij

机构信息

Institute of Physiology and Pathophysiology and Interdisciplinary Center for Neurosciences (IZN), University of Heidelberg, Im Neuenheimer Feld 326, D-69120 Heidelberg, Germany.

出版信息

Prog Brain Res. 2007;160:245-59. doi: 10.1016/S0079-6123(06)60014-9.

DOI:10.1016/S0079-6123(06)60014-9

PMID:17499118

Abstract

Presynaptic receptors provide plasticity to GABAergic synapses in the basal ganglia network, in which GABA neurons outnumber all other neurons. Presynaptic receptors, mostly of the metabotropic type, enhance or reduce the strength of synaptic inhibition and are activated by ligands being released from the GABA terminals themselves (autoreceptors) or by ligands coming from other sources (heteroreceptors), including the target neurons innervated by the GABA terminals. The latter mechanism, termed retrograde signaling, is given particular emphasis as far as it occurs in substantia nigra.

摘要

突触前受体为基底神经节网络中的GABA能突触提供可塑性，其中GABA能神经元的数量超过所有其他神经元。突触前受体大多为代谢型，可增强或降低突触抑制的强度，并被从GABA能终末自身释放的配体（自身受体）或来自其他来源的配体（异源受体）激活，这些来源包括GABA能终末所支配的靶神经元。后一种机制，即逆行信号传递，因其在黑质中发生而受到特别强调。