PRESYNAPTIC MECHANISMS IN HAIR CELLS

这项研究的长期目标是了解机制 在快速突触传递过程中潜在的钙离子介导的胞吐作用。 化学突触是塑料的常见表现部位 改变思想，以支持某些形式的学习、记忆和 中枢神经系统的发育变化。此外，突触 也是许多神经活性物质的靶标，如毒素和 治疗药物，并可在某些类型的 神经病理学。因此，对突触功能的更好理解 这对医学科学的进步很可能是至关重要的。其作用机制 潜在的胞吐作用将在青蛙的毛细胞中进行研究。 球囊。这些细胞非常适合研究突触。 机制，特别是钙离子和钙结合蛋白的作用 (calbindin-D28k和synaptopagmin)与胞吐作用有关。具体目标是： (1)验证流动钙缓冲钙结合蛋白-D28k的假设 影响青蛙球囊毛细胞的短程钙信号。(2) 要检验这样一种假设，即由 去极化是由于突触小泡与血浆的融合。 活动区的细胞膜。这项工作将提供定量的信息 关于钙信号和神经递质的释放 适用于神经系统中的其他突触。

The long-term objective of this study is to understand mechanisms underlying Ca2+-mediated exocytosis during fast synaptic transmission. Chemical synapses are common sites for the manifestation of plastic changes thought to underlie some forms of learning, memory and developmental changes in the central nervous system. Moreover, synapses are also the targets of many neuroactive agents such as toxins and therapeutic drugs, and can become dysfunctional in certain types of neuropathology. A better understanding of synaptic function is therefore likely to be vital for advances in medical science. The mechanisms underlying exocytosis will be investigated in hair cells from the frog sacculus. These cells are ideally suited for the study of synaptic mechanisms, particularly the roles of Ca2+ and Ca2+-binding proteins (calbindin-D28k and synaptotagmin) in exocytosis. The specific aims are: (1) To test the hypothesis that the mobile Ca2+ buffer calbindin-D28k influences short-range Ca2+ signaling in frog saccular hair cells. (2) To test the hypothesis that increases in membrane capacitance induced by depolarization are due to the fusion of synaptic vesicles with the plasma membrane at active zones. This work will provide quantitative information about Ca2+ signaling and the release of neurotransmitter that should be applicable to other synapses in the nervous system.