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GSK-3β activity and hyperdopamine-dependent behaviors
Journal article   Open access   Peer reviewed

GSK-3β activity and hyperdopamine-dependent behaviors

Yan-Chun Li and Wen-Jun Gao
Neuroscience and biobehavioral reviews, v 35(3), pp 645-654
Jan 2011
PMID: 20727368
url
https://doi.org/10.1016/j.neubiorev.2010.08.001View
Published, Version of Record (VoR) Open

Abstract

Animals Receptors, Dopamine - metabolism Humans Glycogen Synthase Kinase 3 beta Nervous System Diseases - metabolism Signal Transduction - physiology Nervous System Diseases - physiopathology Glycogen Synthase Kinase 3 - metabolism Dopamine - metabolism
Dopamine plays important roles in normal brain function and many neuropsychiatric disorders. Classically, dopamine receptors are positively coupled to G protein-mediated signaling to regulate cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA)-dopamine and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and Ca(2+) pathways. However, emerging evidence indicates that under hyperdopaminergic conditions, the protein kinase B (Akt)-glycogen synthase kinase 3β (GSK-3β) signaling cascade may mediate dopamine actions via D(2)-like receptors. This cAMP-independent signaling pathway involves the regulation of downstream synaptic targets, e.g., AMPA receptor, NMDA receptors, and thus synaptic plasticity. Here we provide an overview of how this novel signaling pathway relays dopamine receptor-mediated responses, particularly hyperdopamine-dependent behaviors. We discuss the relevance of the Akt/GSK-3β signaling cascade for the expression of dopamine-dependent behaviors and the drug actions associated with dopaminergic systems.

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Web of Science research areas
Behavioral Sciences
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