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Brain Res. 2015 Dec 2;1628(Pt A):17-28. doi: 10.1016/j.brainres.2015.06.037. Epub 2015 Jul 14.

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

Author information

1
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, MD 21205, USA. Electronic address: tanya.marton@gmail.com.
2
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, MD 21205, USA. Electronic address: shuler@jhmi.edu.
3
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, MD 21205, USA. Electronic address: pworley@jhmi.edu.

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.

KEYWORDS:

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

PMID:
26187757
DOI:
10.1016/j.brainres.2015.06.037
[Indexed for MEDLINE]

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