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. 1999 Jan;22(1):147-56.
doi: 10.1016/s0896-6273(00)80686-8.

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

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Free article

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

D G Chain et al. Neuron. 1999 Jan.
Free article

Abstract

The formation of a persistently active cAMP-dependent protein kinase (PKA) is critical for 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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