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Lack of effect of N ω ‐nitro‐ L ‐arginine methyl ester on bromocriptine‐induced locomotor sensitization in mice
Author(s) -
Kayir Hakan,
Ceyhan Mert,
Yavuz Oğuzhan,
Uzbay I. Tayfun
Publication year - 2007
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20440
Subject(s) - bromocriptine , sensitization , chemistry , pharmacology , locomotor activity , arginine , nitro , behavioral sensitization , stereochemistry , neuroscience , medicine , biochemistry , biology , amino acid , organic chemistry , prolactin , hormone , receptor , alkyl , nucleus accumbens
The present study was designed to investigate the effects of N ω ‐nitro‐ L ‐arginine methyl ester ( L ‐NAME), a nitric oxide (NO) synthase inhibitory agent, on bromocriptine‐induced locomotor sensitization in mice. Adult male Swiss‐Webster mice (26–32 g) were the subjects. Saline or L ‐NAME (15–60 mg/kg) was injected to mice intraperitoneally 30 min before bromocriptine (5 mg/kg), and locomotor activity was recorded for 240 min in an open field activity monitoring system. This procedure lasted for 2 weeks, once in 2 days from Monday to Friday, six sessions in total. After a 2‐day drug‐free period, a challenge injection of bromocriptine (5 mg/kg) or vehicle was administered by all groups of mice. Other groups of mice treated with bromocriptine according to the aforementioned procedure except L ‐NAME pretreatments were challenged with saline or L ‐NAME (15–60 mg/kg) plus bromocriptine (5 mg/kg) after a 2‐day drug‐free period. Bromocriptine produced a significant locomotor sensitization. L ‐NAME (15–60 mg/kg) did not have any significant effect on the development and expression of bromocriptine‐induced locomotor sensitization in mice. Meanwhile, the data also imply that NO‐related mechanisms may not be responsible for bromocriptine‐induced locomotor sensitization in mice. Synapse 61:869–874, 2007. © 2007 Wiley‐Liss, Inc.