Littleton J T, Bellen H J
Howard Hughes Medical Institute, Dept of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Trends Neurosci. 1995 Apr;18(4):177-83. doi: 10.1016/0166-2236(95)93898-8.
Although numerous electrophysiological and biochemical studies have defined many of the properties of the putative Ca2+ receptor for exocytosis at the synapse, the molecular mechanisms that couple influx of Ca2+ and release of neurotransmitter have remained elusive. Several proteins have emerged recently as putative Ca2+ sensors. Interestingly, one of these proteins, synaptotagmin, shares many properties with the putative Ca2+ receptor. Recent genetic experiments in Caenorhabditis elegans, Drosophila and mouse have provided important insights about synaptotagmin's role in neurotransmitter release. These experiments, combined with electrophysiological and biochemical studies, suggest that synaptotagmin is a key Ca2+ sensor, converting the ubiquitously used cellular secretory pathway into a Ca(2+)-regulated exocytotic pathway.
尽管众多电生理和生化研究已经明确了突触处假定的用于胞吐作用的Ca2+受体的许多特性，但将Ca2+内流与神经递质释放相偶联的分子机制仍然不清楚。最近有几种蛋白质作为假定的Ca2+传感器出现。有趣的是，其中一种蛋白质——突触结合蛋白，与假定的Ca2+受体具有许多共同特性。最近在秀丽隐杆线虫、果蝇和小鼠中进行的遗传学实验为突触结合蛋白在神经递质释放中的作用提供了重要见解。这些实验与电生理和生化研究相结合，表明突触结合蛋白是一种关键的Ca2+传感器，将普遍使用的细胞分泌途径转变为Ca(2+)-调节的胞吐途径。
