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1.
Indian J Physiol Pharmacol ; 1986 Jan-Mar; 30(1): 85-90
Article in English | IMSEAR | ID: sea-107291

ABSTRACT

Bromocriptine (5-30 mg/kg, ip), 2 hr after administration, induced cage climbing behaviour in mice. Pretreatment with haloperidol, an antagonist of both D-1 and D-2 dopamine receptors, metoclopramide and molindone, the selective D-2 dopamine receptor antagonists, effectively antagonised bromocriptine-induced climbing behaviour. The results indicate that bromocriptine most probably induces climbing behaviour in mice by stimulating the postsynaptic striatal D-2 dopamine receptors.


Subject(s)
Animals , Behavior, Animal/drug effects , Bromocriptine/antagonists & inhibitors , Dose-Response Relationship, Drug , Haloperidol/pharmacology , Male , Metoclopramide/pharmacology , Mice , Molindone/pharmacology , Motor Activity/drug effects , Receptors, Dopamine/drug effects , Receptors, Dopamine D2
2.
Indian J Physiol Pharmacol ; 1984 Oct-Dec; 28(4): 326-30
Article in English | IMSEAR | ID: sea-107020

ABSTRACT

Pretreatment with fenfluramine (5 and 10 mg/kg, ip) in doses which induced head twitches was found to antagonize apomorphine-induced cage climbing behaviour and methamphetamine stereotypy in mice. Since fenfluramine (5 and 10 mg/kg) did not induce catalepsy it indicates that fenfluramine lacks postsynaptic striatal and mesolimbic dopamine receptor blocking activity and it is possible that the fenfluramine-induced enhancement of central 5-hydroxytryptamine neuronal transmission may be responsible for its antagonistic effect on apomorphine-induced climbing behaviour and methamphetamine stereotypy.


Subject(s)
Animals , Apomorphine/antagonists & inhibitors , Catalepsy/chemically induced , Fenfluramine/pharmacology , Humans , Male , Methamphetamine/antagonists & inhibitors , Mice , Stereotyped Behavior/drug effects
4.
Indian J Physiol Pharmacol ; 1983 Jul-Sep; 27(3): 241-4
Article in English | IMSEAR | ID: sea-108832

ABSTRACT

Pretreatment with alpha-methyl-p-tyrosine, a tyrosine hydroxylase inhibitor, was found to increase the intensity of catalepsy induced by haloperidol, chlorpromazine and molindone. The drug probably decreases the synthesis of dopamine and makes less dopamine available for release and to compete with the neuroleptic for the postsynaptic striatal dopamine receptor sites with resultant potentiation of the neuroleptic-induced catalepsy.


Subject(s)
Animals , Antipsychotic Agents/toxicity , Catalepsy/chemically induced , Chlorpromazine/toxicity , Dopamine/biosynthesis , Drug Synergism , Haloperidol/toxicity , Humans , Male , Methyltyrosines/toxicity , Molindone/toxicity , Rats , alpha-Methyltyrosine
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