Induction and maintenance mechanism of late phase of cerebellar synaptic plasticity

小脑的突触可塑性被认为是运动学习的细胞基础。颗粒神经元和浦肯野神经元之间兴奋性突触的长期抑制(LTD)和中间神经元和浦肯野神经元之间的抑制性突触的反弹增强(RP)已有报道。突触可塑性由转录非依赖的早期阶段和转录依赖的晚期阶段组成。在本研究中，我们通过测量小脑培养的微小兴奋性或抑制性突触后电流(mEPSC，mIPSC)来研究突触可塑性晚期的表达和维持机制。我们发现，抑制钙调神经磷酸酶(一种钙和钙调蛋白依赖的蛋白磷酸酶)可以诱导LTD的晚期。我们的结果表明，超氧化物下调钙调神经磷酸酶触发了浦肯野神经元LTD晚期的诱导。我们还成功地演示了RP的整个时间过程。RP还包括持续一天以上的早期阶段和转录依赖的晚期阶段。

The synaptic plasticity in the cerebellum has been considered as a cellular basis of motor learning. Long-term depression (LTD) at excitatory synapses between a granule neuron and a Purkinje neuron and rebound potentiation (RP) at inhibitory synapses between an interneuron and a Purkinje neuron, has been reported. The synaptic plasticity is composed of transcription-independent early phase and transcription-dependent late phase. In this study, we have studied the expression and maintenance mechanism of late phase of synaptic plasticity utilizing measurement of miniature excitatory or inhibitory postsynaptic current (mEPSC, mIPSC) in the rat cerebellar culture. We found that inhibition of calcineurin (a calcium and calmodulin dependent protein phosphatase) induced the late phase of LTD. Our results suggest that down regulation of calcineurin by superoxide triggers the induction of late phase of LTD in a Purkinje neuron. We also succeeded to demonstrate whole time course of RP. RP also consisted of early phase and transcription-dependent late phase lasting for more than a day.