摘要
程序性细胞死亡是多细胞机体在发育过程中调控机体正常生理功能的重要机制。日益增多的证据表明，某些中枢神经系统疾病的发生与发展涉及到神经元的程序性死亡。应用体外去极化条件下，原代培养的小脑颗粒神经元，经复极化处理，可以诱导典型的神经元程序性死亡。研究发现，小脑中广泛存在的神经递质谷氨酸和乙酰胆碱，可以通过特异性的受体调节神经元的程序性死亡。从而提示，神经递质在传导神经冲动的同时，也特异性地传导神经元的生存信号。进一步的实验证明，激活不同的Ｇ蛋白（Ｇｓ或Ｇｉ／ｏ）可以阻断或者诱导神经元的程序性死亡，提示Ｇ蛋白在神经元程序性死亡信号的跨膜传导过程中可能发挥双向开关的作用。某些神经系统药物（如苯妥英钠）和神经毒素（如胆红素）引起小脑萎缩的机制也可能与颗粒神经元的程序性死亡有关。
Programmed cell death is an important mechanism responsible for the regulation of physiological function during development. There is increasing evidence that programmed neuronal death is involved in occurrence and development of pathological CNS insult. If in vitro cultured cerebellar granule neurons under depolarization are exposed to nondepolarizing culture condition they will die via programmed cell death. Glutamate and acetylcholine, as the primary neurotransmitters in cerebellar granule neurons, can regulate programmed cell death of neurons via their specific receptors, which suggests that neurotransmitters may not only mediate synapatic transmission of neuronal impulses but also transduce the survival signals for some neurons. The further experiments show that activation of different Gprotein (Gs or Gi/o) blocks or induces programmed neuronal death, suggesting that Gprotein may function as key switches for controlling the programmed neuronal death. Some of CNS drugs (such as diphenylhydantoin) and neurotoxins (such as bilirubin) induce cerebellar atrophy via programmed death of granule neurons.
出处
《中山医科大学学报》
CSCD
1998年第1期1-3,共3页
Academic Journal of Sun Yat-sen University of Medical Sciences
