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The antimanic‐like effect of phenytoin and carbamazepine on methylphenidate‐induced hyperlocomotion: role of voltage‐gated sodium channels
Author(s) -
Tonelli Denise A.G.,
Pereira Marcela,
Siba Isadora P.,
Martynhak Bruno J.,
Correia Diego,
Casarotto Plínio C.,
Biojone Caroline,
Guimarães Francisco S.,
Joca Samia L.R.,
Andreatini Roberto
Publication year - 2013
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/fcp.12022
Subject(s) - carbamazepine , phenytoin , chemistry , methylphenidate , sodium channel , pharmacology , anticonvulsant , sodium , epilepsy , medicine , attention deficit hyperactivity disorder , organic chemistry , psychiatry
The objective of this study was to verify whether phenytoin modifies methylphenidate‐induced hyperlocomotion, an animal model for screening antimanic‐like drugs, and also evaluate the effect of veratrine, a voltage‐gated sodium channel opener, pretreatment on the effect of phenytoin in this model. Carbamazepine was used as a positive control. Methylphenidate (5 mg/kg, s.c.) increased open‐field locomotion, and phenytoin (5–10 mg/kg, i.p.) and carbamazepine (20 mg/kg, i.p.) blocked this effect. Veratrine (0.4 mg/kg, s.c.) pretreatment reversed the effects of phenytoin (10 mg/kg, i.p.) and carbamazepine (20 mg/kg, i.p.). Phenytoin (1–50 mg/kg, i.p.) and carbamazepine (10–20 mg/kg i.p.) alone did not change spontaneous locomotor activity. These results indicate that voltage‐gated sodium channels play an important role in antimanic‐like effects of phenytoin and carbamazepine on psychostimulant‐induced hyperlocomotion model.