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Microinjection of the L-type calcium channel antagonist diltiazem into the ventral nucleus accumbens shell facilitates cocaine-induced conditioned place preferences.
Chartoff, Elena H; Pliakas, Andrea M; Carlezon, William A.
Afiliação
  • Chartoff EH; Behavioral Genetics Laboratory, Department of Psychiatry, Harvard Medical School, McLean Hospital, Belmont, Massachusetts 02478, USA.
Biol Psychiatry ; 59(12): 1236-9, 2006 Jun 15.
Article em En | MEDLINE | ID: mdl-16458265
BACKGROUND: Calcium (Ca2+) influx within the nucleus accumbens shell (NASh) can influence brain reward processes. We found previously that rats self-administer NMDA receptor antagonists (which block Ca2+ influx through NMDA receptors) into the NASh. We also found that manipulations which increase expression of Ca2+-permeable AMPA receptors within this region make cocaine aversive. Here we examined if Ca2+ influx via L-type Ca2+ channels within the NASh would influence cocaine reward. METHODS: Rats received bilateral microinjections of the L-type Ca2+ channel antagonist diltiazem into the ventral NASh prior to place conditioning with systemic cocaine. RESULTS: Microinjections of diltiazem (10 nmol/hemisphere) into the ventral NASh facilitated the ability of a sub-threshold dose of cocaine (5.0 mg/kg) to establish place preferences, but did not affect place conditioning on their own (5.0-40 nmol/hemisphere). Microinjections into more dorsal regions had no effects. CONCLUSIONS: Blockade of Ca2+ influx through L-type channels Ca2+ within the ventral NASh increases cocaine reward.
Assuntos
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Base de dados: MEDLINE Assunto principal: Bloqueadores dos Canais de Cálcio / Diltiazem / Comportamento de Escolha / Cocaína / Condicionamento Operante / Núcleo Accumbens Limite: Animals Idioma: En Ano de publicação: 2006 Tipo de documento: Article
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Base de dados: MEDLINE Assunto principal: Bloqueadores dos Canais de Cálcio / Diltiazem / Comportamento de Escolha / Cocaína / Condicionamento Operante / Núcleo Accumbens Limite: Animals Idioma: En Ano de publicação: 2006 Tipo de documento: Article