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Provedor de dados:  BJMBR
País:  Brazil
Título:  Acute buspirone abolishes the expression of behavioral dopaminergic supersensitivity in mice
Autores:  Queiroz,C.M.T.
Alcântara,F.B.
Yagüe,A.M.L.
Bibancos,T.
Frussa-Filho,R.
Data:  2002-02-01
Ano:  2002
Palavras-chave:  Buspirone
Haloperidol
Dopaminergic supersensitivity
Tardive dyskinesia
Behavior
Mice
Resumo:  Previous studies have shown that rats withdrawn from long-term treatment with dopamine receptor blockers exhibit dopaminergic supersensitivity, which can be behaviorally evaluated by enhanced general activity observed in an open-field. Recently, it has been reported that co-treatment with the non-benzodiazepine anxiolytic buspirone attenuates the development of haloperidol-induced dopaminergic supersensitivity measured by open-field behavior of rats. The aims of the present study were: 1) to determine, as previously reported for rats, if mice withdrawn from long-term neuroleptic treatment would also develop dopaminergic supersensitivity using open-field behavior as an experimental paradigm, and 2) to examine if acute buspirone administration would attenuate the expression of this behavioral dopaminergic supersensitivity. Withdrawal from long-term haloperidol treatment (2.5 mg/kg, once daily, for 20 days) induced a significant (30%) increase in ambulation frequency (i.e., number of squares crossed in 5-min observation sessions) but did not modify rearing frequency or immobility duration in 3-month-old EPM-M1 male mice observed in the open-field apparatus. Acute intraperitoneal injection of buspirone (3.0 and 10 but not 1.0 mg/kg, 12-13 animals per group) 30 min before open-field exposure abolished the increase in locomotion frequency induced by haloperidol withdrawal. These data suggest that the open-field behavior of mice can be used to detect dopaminergic supersensitivity, whose expression is abolished by acute buspirone administration.
Tipo:  Info:eu-repo/semantics/other
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2002000200013
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2002000200013
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.35 n.2 2002
Direitos:  info:eu-repo/semantics/openAccess
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