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[纹状体、新皮层、海马体和小脑中可塑性的统一突触后机制]

[Unified postsynaptic mechanism of plasticity in the striatum, neocortex, hippocampus, and cerebellum].

作者信息

Sil'kis I G

机构信息

Institute of Higher Nervous Activity and Neurophysiology, Russian Acad. Sci., Moscow, Russia.

出版信息

Ross Fiziol Zh Im I M Sechenova. 2000 May;86(5):519-31.

Abstract

The unitary postsynaptic mechanism of plasticity in striatum, neocortex, hippocampus and cerebellum involves the LTP/LTD excitation as result of AMPA and NMDA receptor phosphorylation/dephosphorylation, while the LTP/LTD of inhibition is the result of the GABA receptor phosphorylation/dephosphorylation. It follows from this mechanism that when NMDA channels are closed, the determinant role in receptor phosphorylation is played by the PKG. When the NMDA channels are open, the determinant role in receptor phosphorylation is played by the PKC and CaMKII.

摘要

纹状体、新皮层、海马体和小脑中可塑性的单一突触后机制涉及AMPA和NMDA受体磷酸化/去磷酸化导致的长时程增强/长时程抑制兴奋,而抑制性的长时程增强/长时程抑制是GABA受体磷酸化/去磷酸化的结果。从这一机制可以推断,当NMDA通道关闭时,PKG在受体磷酸化中起决定性作用。当NMDA通道开放时,PKC和CaMKII在受体磷酸化中起决定性作用。

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