Mechanisms for generating the autonomous cAMP-dependent protein kinase required for long-term facilitation in Aplysia

被引：148

作者：

Chain, DG

Casadio, A

Schacher, S

Hegde, AN

Valbrun, M

Yamamoto, N

Goldberg, AL

Bartsch, D

Kandel, ER

Schwartz, JH

机构：

[1] Columbia Univ Coll Phys & Surg, Ctr Neurobiol & Behav, New York, NY 10032 USA

[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA

来源：

NEURON | 1999年 / 22卷 / 01期

关键词：

D O I：

10.1016/S0896-6273(00)80686-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The formation of a persistently active cAMP-dependent protein kinase (PKA) is critical far establishing long-term synaptic facilitation (LTF) in Aplysia. The injection of bovine catalytic (C) subunits into sensory neurons is sufficient to produce protein synthesis-dependent LTF. Early in the LTF induced by serotonin (5-HT), an autonomous PKA is generated through the ubiquitin-proteasome-mediated proteolysis of regulatory (R) subunits. The degradation of R occurs during an early time window and appears to be a key function of proteasomes in LTF. Lactacystin, a specific proteasome inhibitor, blocks the facilitation induced by 5-HT, and this block is rescued by injecting C subunits. R is degraded through an allosteric mechanism requiring an elevation of cAMP coincident with the induction of a ubiquitin carboxy-terminal hydrolase.

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页码：147 / 156

页数：10

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