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Abstract

Locomotor sensitization and decrease in [3H]mazindol binding to the dopamine transporter in the nucleus accumbens are delayed after chronic treatments by GBR12783 or cocaine.

D Boulay, D Duterte-Boucher, I Leroux-Nicollet, L Naudon and J Costentin
Journal of Pharmacology and Experimental Therapeutics July 1996, 278 (1) 330-337;
D Boulay
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D Duterte-Boucher
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I Leroux-Nicollet
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L Naudon
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J Costentin
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Abstract

Rats were treated once daily for 15 consecutive days with either cocaine or the specific dopamine uptake inhibitor 1-[2- (diphenylmethoxy)ethyl]-4-(3-phenyl-2-(propenyl)-piperazine (GBR12783) at a dose (10 mg/kg) that given acutely increases locomotor activity. Two or 14 days after the last administration, the motor stimulant responses of rats to a challenge dose (5 mg/kg) of the drug administered previously were compared with the motor stimulant responses of rats daily injected with solvent. A sensitization to the acute stimulant locomotor effect of these drugs was only observed 14 days after cessation of chronic treatments. After this withdrawal period, autoradiographic analysis revealed a significant decrease in the desipramine-insensitive [3H]mazindol binding to the dopamine transporter in the shell of the nucleus accumbens. No change was noticed in other regions with high dopamine content: core of nucleus accumbens, striatum, olfactory tubercle, substantia nigra and ventral tegmental area. Absence of concomitant decrease in [3H]dihydrotetrabenazine labeling, which indicates lack of effect on vesicular monoamine transporters, suggests that the decrease in accumbal [3H]mazindol binding did not result from a cytotoxic effect on corresponding dopamine neurons. In addition, 14 days after the last administration of GBR12783, the levels of dopamine and metabolites (dihydroxy-phenylacetic acid, homovanillic acid) and the ability of acute GBR12783 to synergize with haloperidol-induced increase in these metabolites were not modified either in the whole nucleus accumbens or in the striatum.

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Journal of Pharmacology and Experimental Therapeutics
Vol. 278, Issue 1
1 Jul 1996
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Abstract

Locomotor sensitization and decrease in [3H]mazindol binding to the dopamine transporter in the nucleus accumbens are delayed after chronic treatments by GBR12783 or cocaine.

D Boulay, D Duterte-Boucher, I Leroux-Nicollet, L Naudon and J Costentin
Journal of Pharmacology and Experimental Therapeutics July 1, 1996, 278 (1) 330-337;

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Abstract

Locomotor sensitization and decrease in [3H]mazindol binding to the dopamine transporter in the nucleus accumbens are delayed after chronic treatments by GBR12783 or cocaine.

D Boulay, D Duterte-Boucher, I Leroux-Nicollet, L Naudon and J Costentin
Journal of Pharmacology and Experimental Therapeutics July 1, 1996, 278 (1) 330-337;
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