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Title: The reboxetine-induced increase of accumbal dopamine efflux is inhibited by l-propranolol: a microdialysis study with freely moving rats.
Author(s): Mizoguchi, N.
Saigusa, T.
Aono, Y.
Sekino, R.
Takada, K.
Oi, Y.
Ueda, K.
Koshikawa, N.
Cools, A.R. (068808399)
Publication year: 2008
Document type: Article / Letter to editor
Journal: European Journal of Pharmacology
ISSN: 0014-2999
Volume: vol. 601
Issue: iss. 1-3
Start page: p. 94
End page: p. 98
Abstract: In vivo microdialysis was used to study the effects of the locally applied selective noradrenaline uptake inhibitor reboxetine on the baseline noradrenaline and dopamine efflux in the nucleus accumbens of freely moving rats. The effects of intra-accumbal infusion of the beta-adrenoceptor antagonist l-propranolol on the reboxetine-elicited noradrenaline and dopamine efflux in the nucleus accumbens were also analysed. The intra-accumbal infusion of reboxetine (1.2 and 12 pmol) significantly increased both the accumbal noradrenaline efflux and the accumbal dopamine efflux. The intra-accumbal infusion of the chosen doses of l-propranolol (300 and 1200 pmol) did not alter the accumbal noradrenaline and dopamine efflux. The l-propranolol treatment did not affect the reboxetine-elicited accumbal noradrenaline efflux, but it significantly inhibited the reboxetine-elicited increase of accumbal dopamine efflux. The doses mentioned are the total amount of drug over the infusion period that varied across the drugs (60 or 120 min). The present study shows that the intra-accumbal infusion of selective noradrenaline uptake inhibitor reboxetine increases noradrenaline as well as dopamine efflux in the nucleus accumbens of freely moving rats. This study also indicates that inhibition of accumbal beta-adrenoceptors prevented the increase of the reboxetine-induced accumbal dopamine efflux. It is suggested that the reboxetine-induced increase of the endogenous accumbal noradrenaline activates among others accumbal beta-adrenoceptors that, in turn, stimulate the accumbal release of dopamine.
Subject: UMCN 3.2: Cognitive neurosciences
Organization: Cognitive Neuroscience
Psychoneuropharmacology
UMCN Extern
Organization (former): Medical Physics and Biophysics
Appears in Collections:Academic bibliography

Please use this identifier to cite or link to this item: http://hdl.handle.net/2066/70690

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