Tempia F, Konnerth A
I. Physiologisches Institut, Universität des Saarlandes, Homburg, Germany.
Semin Cell Biol. 1994 Aug;5(4):243-50. doi: 10.1006/scel.1994.1030.
Cerebellar Purkinje neurons (PNs) receive two main excitatory inputs, from climbing fibers and parallel fibers, and inhibitory inputs, from GABAergic interneurons. The synapses formed by parallel fibers and by inhibitory interneurons on PNs are able to undergo long-lasting changes in efficacy. Thus, the excitatory parallel fiber-PN synapse undergoes long-term depression when it is activated in conjunction with climbing fibers. Synaptic inhibition can be potentiated by climbing fiber activity by a mechanism named rebound potentiation, resulting in a more powerful inhibitory effect of GABAergic interneurons. The induction of both long-term depression and rebound potentiation requires a transient elevation of the cytoplasmic calcium concentration ([Ca2+]i). The [Ca2+]i-transient is caused by Ca2+ entry through voltage-gated Ca2+ channels and, possibly, by release of Ca2+ from IP3- and ryanodine-sensitive stores. Direct Ca2+ entry through synaptic AMPA receptor channels seems not to contribute significantly to the Ca2+ signal mediating the induction of both long-term depression and rebound potentiation.
小脑浦肯野神经元（PNs）接收两种主要的兴奋性输入，分别来自攀缘纤维和平行纤维，以及抑制性输入，来自γ-氨基丁酸（GABA）能中间神经元。平行纤维和抑制性中间神经元在浦肯野神经元上形成的突触能够发生效能的长期变化。因此，当兴奋性平行纤维-浦肯野神经元突触与攀缘纤维共同激活时，会经历长时程抑制。通过一种名为反弹增强的机制，攀缘纤维活动可增强突触抑制，从而使GABA能中间神经元产生更强的抑制作用。长时程抑制和反弹增强的诱导都需要细胞质钙浓度（[Ca2+]i）的短暂升高。[Ca2+]i瞬变是由Ca2+通过电压门控Ca2+通道进入引起的，也可能是由IP3和兰尼碱敏感储存库释放Ca2+引起的。通过突触α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体通道直接进入的Ca2+似乎对介导长时程抑制和反弹增强诱导的Ca2+信号没有显著贡献。
