Role of proteasome-dependent protein degradation in long-term operant memory in Aplysia

Learn Mem. 2016 Dec 15;24(1):59-64. doi: 10.1101/lm.043794.116. Print 2017 Jan.

Abstract

We investigated the in vivo role of protein degradation during intermediate (ITM) and long-term memory (LTM) in Aplysia using an operant learning paradigm. The proteasome inhibitor MG-132 inhibited the induction and molecular consolidation of LTM with no effect on ITM. Remarkably, maintenance of steady-state protein levels through inhibition of protein synthesis using either anisomycin or rapamycin in conjunction with proteasome inhibition permitted the formation of robust 24 h LTM. Our studies suggest a primary role for proteasomal activity in facilitation of gene transcription for LTM and raise the possibility that synaptic mechanisms are sufficient to sustain 24 h memory.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Analysis of Variance
  • Animals
  • Anisomycin / pharmacology
  • Aplysia / drug effects
  • Aplysia / physiology*
  • Conditioning, Operant / drug effects
  • Conditioning, Operant / physiology*
  • Cysteine Proteinase Inhibitors / pharmacology
  • Leupeptins / pharmacology
  • Memory, Long-Term / drug effects
  • Memory, Long-Term / physiology*
  • Proteasome Endopeptidase Complex / drug effects
  • Proteasome Endopeptidase Complex / metabolism*
  • Time Factors

Substances

  • Cysteine Proteinase Inhibitors
  • Leupeptins
  • Anisomycin
  • Proteasome Endopeptidase Complex
  • benzyloxycarbonylleucyl-leucyl-leucine aldehyde