Inhibition of GSK3 attenuates dopamine D1 receptor agonist-induced hyperactivity in mice

Abstract Recent evidence suggests a critical role for the intracellular signaling protein glycogen synthase kinase-3 (GSK3) in hyperactivity associated with dopaminergic transmission. Here, we investigated whether activation of GSK3 is necessary for the expression of behaviors specifically produced...

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Bibliographic Details
Published in:Brain research bulletin 2010-05, Vol.82 (3), p.184-187
Main Authors: Miller, Jonathan S, Tallarida, Ronald J, Unterwald, Ellen M
Format: Article
Language:English
Subjects:
Activity
Ambulation
Animals
Behavior, Animal - drug effects
Benzazepines - pharmacology
Dopamine
Dopamine Agonists - pharmacology
Dose-Response Relationship, Drug
Glycogen Synthase Kinase 3 - antagonists & inhibitors
Glycogen Synthase Kinase 3 - metabolism
Glycogen synthase kinase-3
Hyperkinesis - chemically induced
Indoles - pharmacology
Male
Maleimides - pharmacology
Mice
Motor Activity - drug effects
Neurology
Receptors, Dopamine D1 - metabolism
Stereotypy
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Summary:Abstract Recent evidence suggests a critical role for the intracellular signaling protein glycogen synthase kinase-3 (GSK3) in hyperactivity associated with dopaminergic transmission. Here, we investigated whether activation of GSK3 is necessary for the expression of behaviors specifically produced by dopamine D1 receptor activation. To assess the role of GSK3 in dopamine D1 receptor-induced hyperactivity, mice were pretreated with the selective GSK3 inhibitor SB 216763 (0.25–7.5 mg/kg, i.p.) or its vehicle prior to administration of the dopamine D1 receptor full-agonist SKF-82958 (1.0 mg/kg, i.p.) or saline control. Inhibition of GSK3 via SB 216763 dose-dependently reduced ambulatory and stereotypic activity produced by SKF-82958. These data implicate a role for GSK3 in the behavioral manifestations associated with dopamine D1 receptor activation.
ISSN:0361-9230
1873-2747
DOI:10.1016/j.brainresbull.2010.03.005