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Long-term depression and other synaptic plasticity in the cerebellum

机译:小脑的长期抑郁和其他突触可塑性

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摘要

Cerebellar long-term depression (LTD) is a type of synaptic plasticity and has been considered as a critical cellular mechanism for motor learning. LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to transmitter glutamate. Molecular induction mechanism of LTD has been intensively studied using culture and slice preparations, which has revealed critical roles of Ca2+, protein kinase C and endocytosis of AMPA-type glutamate receptors. Involvement of a large number of additional molecules has also been demonstrated, and their interactions relevant to LTD mechanisms have been studied. In vivo experiments including those on mutant mice, have reported good correlation of LTD and motor learning. However, motor learning could occur with impaired LTD. A possibility that cerebellar synaptic plasticity other than LTD compensates for the defective LTD has been proposed.
机译:小脑长期抑郁症(LTD)是一种突触可塑性,被认为是运动学习的关键细胞机制。 LTD发生在小脑皮层中平行纤维与Purkinje细胞之间的兴奋性突触中,并表示为对递质谷氨酸的应答性降低。通过培养和切片制备方法对LTD的分子诱导机理进行了深入研究,揭示了Ca 2 + ,蛋白激酶C和AMPA型谷氨酸受体内吞作用的关键作用。还证明了大量其他分子的参与,并且已经研究了它们与LTD机制相关的相互作用。体内实验,包括对突变小鼠的实验,已经报告了LTD与运动学习的良好关联。但是,运动障碍可能会因LTD受损而发生。已经提出了除LTD以外的小脑突触可塑性补偿有缺陷的LTD的可能性。

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