Molecular Mechanisms of Early and Late LTP

Neurochem Res. 2019 Feb;44(2):281-296. doi: 10.1007/s11064-018-2695-4. Epub 2018 Dec 6.

Abstract

LTP is the most intensively studied cellular model of the memory and generally divided at least two distinct phases as early and late. E-LTP requires activation of CaMKII that initiates biochemical events and trafficking of proteins, which eventually potentiate synaptic transmission, and is independent of de novo protein synthesis. In contrast, L-LTP requires gene expression and local protein synthesis regulated via TrkB receptor- and functional prions CPEB2-3-mediated translation. Maintenance of LTP for longer periods depends on constitutively active PKMζ. Throughout this review, current knowledge about early and late phases of LTP will be reviewed.

Keywords: Cpeb; Functional prions; Learning and memory; Ltp; Pkm zeta; Synaptic plasticity.

Publication types

  • Review

MeSH terms

  • Animals
  • Hippocampus / metabolism*
  • Humans
  • Long-Term Potentiation / immunology*
  • Long-Term Potentiation / physiology
  • Memory / physiology*
  • Neuronal Plasticity / physiology*
  • Receptor, trkB / metabolism
  • Synaptic Transmission / physiology*

Substances

  • Receptor, trkB