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

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

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Aplysia / metabolism
  • Aplysia / physiology*
  • Cattle
  • Cyclic AMP / physiology
  • Cyclic AMP-Dependent Protein Kinases / biosynthesis*
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Cyclic AMP-Dependent Protein Kinases / pharmacology
  • Cysteine Endopeptidases / physiology
  • Injections
  • Long-Term Potentiation / physiology*
  • Multienzyme Complexes / physiology
  • Neurons, Afferent / drug effects
  • Neurons, Afferent / physiology
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology
  • Proteasome Endopeptidase Complex
  • Serotonin / pharmacology
  • Ubiquitins / metabolism

Substances

  • Multienzyme Complexes
  • Peptide Fragments
  • Ubiquitins
  • Serotonin
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinases
  • Cysteine Endopeptidases
  • Proteasome Endopeptidase Complex