L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum.

L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum. Research Abstract Details 

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L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum. Abstract Text:

J Lee,W J Rushlow,N Rajakumar,J Lee,W J Rushlow,N Rajakumar,J Lee,W J Rushlow,N Rajakumar,J Lee,W J Rushlow,N Rajakumar,

Haloperidol-induced c-Fos expression in the lateral part of the neostriatum has been correlated with motor side effects while c-Fos induction in the medial part of the neostriatum and the nucleus accumbens is thought to be associated with the therapeutic effects of the drug. Induction of c-Fos in the striatum by haloperidol involves dopamine D(2) (DA D(2)) receptor antagonism and is dependent on activation of N-methyl-d-aspartate (NMDA) receptors and L-type Ca(2+) channels. In the current study, pretreatment with L-type Ca(2+) channel blockers suppressed haloperidol-induced c-Fos throughout the neostriatum and the nucleus accumbens at 2 h postinjection. However, elevated c-Fos protein expression was observed only in the lateral part of the neostriatum at 5 h postinjection of haloperidol following pretreatment of L-type Ca(2+) channel blocker compared with rats pretreated with vehicle alone. In addition, pretreatment prolonged the duration of haloperidol-induced catalepsy in rats. Infusions of L-type Ca(2+) channel blockers directly into the neostriatum mimicked similar patterns of changes in haloperidol-induced c-Fos expression. Prolonged expression of c-Fos was not observed following coadministration of nifedipine and a dopamine D(1) (DA D(1)) receptor agonist, SKF 81297, but could be mimicked by the DA D(2/3) receptor antagonist raclopride, suggesting that the phenomenon is likely related to DA D(2) receptor antagonism. Moreover, the expression levels of haloperidol-induced zif 268 and haloperidol-induced phosphorylated CREB and phosphorylated Elk-1 were also substantially elevated for a prolonged period of time in the lateral, but not the medial part of the neostriatum, following blockade of L-type Ca(2+) channels. Collectively, the results suggest that coadministration of L-type Ca(2+) channel blockers affects haloperidol signaling in the lateral part of the neostriatum and may exacerbate the development of acute motor side effects.

L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum. Publishing Authors By Initials

J Lee,WJ Rushlow,N Rajakumar,J Lee,WJ Rushlow,N Rajakumar,J Lee,WJ Rushlow,N Rajakumar,J Lee,WJ Rushlow,N Rajakumar,

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L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Neuroscience

VOLUME: 149

Page Numbers: 602-16

Journal Abbreviation: Neuroscience

ISSN: 0306-4522

DAY: 14

MONTH: 08

YEAR: 2007

L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum. Information

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LANGUAGE: eng

NlmUniqueID: 7605074

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Grant and Affiliation Information for L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum.

AFFILIATION: Department of Anatomy & Cell Biology, University of Western Ontario, London, Ontario N6A 5C1, Canada.

Country: United States

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MEDLINETA: Neuroscience

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