Daniel H, Levenes C, Crépel F
Institut des Neurosciences, CNRS-Université Paris VI, France.
Trends Neurosci. 1998 Sep;21(9):401-7. doi: 10.1016/s0166-2236(98)01304-6.
In the past decade there have been advances in understanding the cellular mechanisms of the long-term depression (LTD) of synaptic transmission at parallel fiber-Purkinje cell synapses in the cerebellum. This review first summarizes current views on mechanisms involved in LTD induction, from activation of voltage-gated Ca2+ channels, of ionotropic (AMPA) and metabotropic (mGluRI) glutamate receptors, to stimulation of protein kinase C and nitric oxide formation. Second, we will focus on recent findings that point towards the involvement of Ca2+ release from internal stores in LTD induction, localize the sources and targets of nitric oxide and indicate a postsynaptic site for LTD expression. Finally, a role for LTD in motor learning is now well supported by recent experiments on transgenic mice.
在过去十年中,人们对小脑平行纤维-浦肯野细胞突触处突触传递的长期抑制(LTD)的细胞机制有了进一步的认识。本综述首先总结了目前关于LTD诱导机制的观点,从电压门控Ca2+通道的激活、离子型(AMPA)和代谢型(mGluRI)谷氨酸受体的激活,到蛋白激酶C的刺激和一氧化氮的形成。其次,我们将关注最近的研究发现,这些发现表明细胞内钙库释放的Ca2+参与了LTD的诱导,确定了一氧化氮的来源和靶点,并指出了LTD表达的突触后位点。最后,最近对转基因小鼠的实验充分支持了LTD在运动学习中的作用。