Lovinger D M, Tyler E
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Noshville, Tennessee 37232, USA.
Int Rev Neurobiol. 1996;39:77-111. doi: 10.1016/s0074-7742(08)60664-9.
The neostriatum is the entryway into the basal ganglia and is the site of many of the neurological defects involving basal ganglia function. Thus, it is important to understand the regulation of synaptic transmission at afferent synapses innervating the neostriatum. Cortical glutamatergic and nigral dopaminergic afferent input impinge on neurons in the neostriatum, providing the most significant afferent inputs to this structure. Our understanding of the mechanisms involved in transmission and modulation of transmission at these synapses has greatly increased. It is now apparent that the corticostriatal glutamatergic inputs produce rapid depolarization of striatal neurons via activation of ionotropic AMPA-type glutamate receptors. In addition, transmission is modulated by a number of presynaptic, G-protein-coupled receptors but, surprisingly, relatively little evidence of postsynaptic modulation has been observed. Corticostriatal synapses also express certain forms of plasticity, most notably short- and long- term synaptic depression (STI) and LTD, respectively). It appears that LTD may involve convergent actions of glutamate and dopamine. Striatal LTD may have important roles in information storage and motor set selection in the striatum. However, some aspects of synaptic transmission in the striatum remain unclear. In particular, the exact physiological roles of dopaminergic nigrostriatal input and the role of NMDA-type glutamate receptors are not well understood. In addition, intrastriatal synaptic connections have received relatively little attention as compared with extrinsic input to the neostriatum. Future studies will need to focus on elucidating these aspects of neostriatal function.
新纹状体是进入基底神经节的入口，也是许多涉及基底神经节功能的神经缺陷的发生部位。因此，了解支配新纹状体的传入突触处的突触传递调节非常重要。皮质谷氨酸能和黑质多巴胺能传入输入作用于新纹状体中的神经元，为该结构提供了最重要的传入输入。我们对这些突触处传递及传递调节机制的理解有了很大提高。现在很明显，皮质纹状体谷氨酸能输入通过激活离子型AMPA型谷氨酸受体使纹状体神经元快速去极化。此外，传递受到多种突触前G蛋白偶联受体的调节，但令人惊讶的是，突触后调节的证据相对较少。皮质纹状体突触还表现出某些形式的可塑性，最显著的分别是短期和长期突触抑制（STI和LTD）。LTD似乎可能涉及谷氨酸和多巴胺的协同作用。纹状体LTD可能在纹状体的信息存储和运动模式选择中起重要作用。然而，纹状体中突触传递的某些方面仍不清楚。特别是，多巴胺能黑质纹状体输入的确切生理作用以及NMDA型谷氨酸受体的作用尚未得到很好的理解。此外，与新纹状体的外部输入相比，纹状体内的突触连接受到的关注相对较少。未来的研究需要集中于阐明新纹状体功能的这些方面。
