Homer 1a and mGluR5 phosphorylation in reward-sensitive metaplasticity: A hypothesis of neuronal selection and bidirectional synaptic plasticity

Research output: Contribution to journalReview article

Abstract

Drug addiction and reward learning both involve mechanisms in which reinforcing neuromodulators participate in changing synaptic strength. For example, dopamine receptor activation modulates corticostriatal plasticity through a mechanism involving the induction of the immediate early gene Homer 1a, the phosphorylation of metabotropic glutamate receptor 5 (mGluR5)′s Homer ligand, and the enhancement of an NMDA receptor-dependent current. Inspired by hypotheses that Homer 1a functions selectively in recently-active synapses, we propose that Homer 1a is recruited by a synaptic tag to functionally discriminate between synapses that predict reward and those that do not. The involvement of Homer 1a in this mechanism further suggests that decaminutes-old firing patterns can define which synapses encode new information. This article is part of a Special Issue entitled SI:Addiction circuits.

Original languageEnglish (US)
Pages (from-to)17-28
Number of pages12
JournalBrain research
Volume1628
DOIs
StatePublished - Dec 2 2015

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Keywords

  • Addiction
  • Dopamine
  • Eligibility trace
  • Homer
  • Immediate early gene
  • NMDA receptor
  • Neuronal selection
  • PIN1
  • Proto weight
  • Provisional weight
  • Reinforcement learning
  • Reward learning
  • Synaptic plasticity
  • Synaptic tag
  • mGluR5

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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