Long-term depression and other synaptic plasticity in the cerebellum.

Long-term depression and other synaptic plasticity in the cerebellum.
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DOI:
10.2183/pjab.89.183
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发表时间:
2013
期刊:
Proceedings of the Japan Academy. Series B, Physical and biological sciences
影响因子:
--
通讯作者:
Hirano T
Hirano T
中科院分区:
其他
文献类型:
--
作者:
Hirano T

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小脑长时程抑制(LTD)是一种突触可塑性,被认为是运动学习的重要细胞机制。LTD发生在平行纤维和小脑皮质中的浦肯野细胞之间的兴奋性突触处,并表现为对递质谷氨酸的反应性降低。LTD的分子诱导机制已通过培养和切片制备进行了深入研究,揭示了Ca 2+、蛋白激酶C和AMPA型谷氨酸受体的内吞作用的关键作用。还证明了大量其他分子的参与,并研究了它们与LTD机制相关的相互作用。包括突变小鼠在内的体内实验已经报道了LTD和运动学习的良好相关性。然而,运动学习可能会发生与受损的有限责任公司的可能性,小脑突触可塑性比有限责任公司补偿缺陷有限责任公司已被提出。
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.
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