Data/hora: 10/06/2024 09:02:22

Provedor de dados: 	56	
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Resumo: 	Previous studies have shown that rats withdrawn from long-term treatment with dopamine receptor blockers exhibit dopaminergic supersensitivity, which can be behaviorally evaluated by enhanced general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 The aims of the present study were: 1) to determine, as previously reported for rats, if mice withdrawn from long-term neuroleptic treatment would also develop dopaminergic supersensitivity using open-field behavior as an experimental paradigm, and 2) to examine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	
Fonte: 	info:eu-repo/semantics/openAccess