Department of Psychiatry and Behavioral Sciences, Nancy Pritzker Laboratory, Stanford University School of Medicine, 1201 Welch Rd. Palo Alto, CA 94304-5485, USA.
Trends Neurosci. 2011 Jun;34(6):326-37. doi: 10.1016/j.tins.2011.03.004. Epub 2011 May 17.
Neurons communicate with one another at specialized contact sites called synapses, composed of pre- and postsynaptic compartments. Presynaptic compartments, or 'boutons', signal to the postsynaptic compartment by releasing chemical neurotransmitter in response to incoming electrical impulses. Recent studies link defects in the function of presynaptic boutons to the etiology of several neurodevelopmental and neurodegenerative diseases, including autism, schizophrenia and Alzheimer's disease. In this review, we describe five core functions of presynaptic boutons and the molecules that mediate these functions, focusing on a subset that are linked to human disease. We also discuss potential mechanisms through which the loss or alteration of these specific molecules could lead to defects in synaptic communication, neural circuit function and, ultimately, cognition and behavior.
神经元在称为突触的专门接触点相互通讯，突触由前突触和后突触隔间组成。前突触隔间，或“末梢”，通过响应传入的电脉冲释放化学神经递质向前突触隔间发出信号。最近的研究将前突触末梢功能的缺陷与几种神经发育和神经退行性疾病的病因联系起来，包括自闭症、精神分裂症和阿尔茨海默病。在这篇综述中，我们描述了前突触末梢的五个核心功能以及介导这些功能的分子，重点介绍了与人类疾病相关的一个子集。我们还讨论了这些特定分子的缺失或改变可能导致突触通讯、神经回路功能以及最终认知和行为缺陷的潜在机制。
