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CNS & Neurological Disorders - Drug Targets


ISSN (Print): 1871-5273
ISSN (Online): 1996-3181

Regulation of Corticostriatal Synaptic Plasticity by G Protein-Coupled Receptors

Author(s): Rakel Lopez de Maturana and Rosario Sanchez-Pernaute

Volume 9, Issue 5, 2010

Page: [601 - 615] Pages: 15

DOI: 10.2174/187152710793361531

Price: $65


Dopamine modulation of excitatory neurotransmission is critical in the control of movement, emotion and reward. In the striatum, medium size spiny neurons (MSNs) are responsible for the integration of cortical and thalamic information that flows through parallel, partly overlapping, loops and determines adequate experience-dependent responses. Dopamine acts on MSNs through two sets of G protein-coupled receptors (GPCRs), the D1-like and D2-like receptors, which can have opposing or synergistic downstream effects. Notably, these two types of striatal dopamine receptors are segregated into the striatonigral (direct) and striatopallidal (indirect) projecting neurons. Thus, dopamine receptor expression determines the morphological and functional neuronal phenotype of MSNs. Moreover, dopamine regulates glutamatergic corticostriatal transmission, critically controlling the induction of long-term potentiation and long-term depression at these synapses, regulating striatal synaptic plasticity. In addition to dopamine receptors, the induction and expression of plasticity mechanisms is regulated by other GPCRs, most importantly adenosine A2A receptors, metabotropic glutamate mGluR5 receptors and endocannabinoid CB1 receptors. This review focuses on synaptic modulation and plasticity on excitatory corticostriatal synapses by GPCRs.

Keywords: Dopamine, glutamate, GPCR, LTP, LTD, Parkinson Disease, plasticity, striatum

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