Homer 1a and mGluR5 phosphorylation in reward-sensitive metaplasticity

A hypothesis of neuronal selection and bidirectional synaptic plasticity

Tanya M. Marton, Marshall Shuler, Paul F Worley

Research output: Contribution to journalArticle

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

Fingerprint

Metabotropic Glutamate 5 Receptor
Neuronal Plasticity
Reward
Phosphorylation
Synapses
Immediate-Early Genes
Dopamine Receptors
N-Methyl-D-Aspartate Receptors
Substance-Related Disorders
Neurotransmitter Agents
Learning
Ligands
Homer Scaffolding Proteins

Keywords

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

ASJC Scopus subject areas

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

Cite this

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title = "Homer 1a and mGluR5 phosphorylation in reward-sensitive metaplasticity: A hypothesis of neuronal selection and bidirectional synaptic plasticity",
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.",
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T2 - A hypothesis of neuronal selection and bidirectional synaptic plasticity

AU - Marton, Tanya M.

AU - Shuler, Marshall

AU - Worley, Paul F

PY - 2015/12/2

Y1 - 2015/12/2

N2 - 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.

AB - 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.

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