Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present experiments was to investigate the locomotor stimulant effects of the atypical antipsychotic agent, clozapine, in rats depleted of their dopamine by reserpine and alpha-methyl-p-tyrosine pretreatment. Clozapine itself induced a slight but never significant stimulation of locomotor activity which was enhanced by the addition of the selective dopamine D1 receptor agonist, SKF38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3- benzazepine), but not by the selective dopamine D2 receptor agonist, quinpirole. The stimulation produced by clozapine plus SKF38393 was blocked by the selective dopamine D1 receptor antagonist, SCH23390 (7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5- tetrahydro-1H-3-benzapine hydrochloride), while the selective dopamine D2 receptor antagonist, haloperidol, was ineffective. A combination of SCH23390 and haloperidol blocked the clozapine plus SKF38393-induced locomotion. Unlike clozapine, neither the selective 5-HT2 receptor antagonist, ritanserin, nor the dopamine D2 receptor antagonists, haloperidol and remoxipride, caused locomotor activation when given alone or in combination with SKF38393. The indirectly acting sympathomimetic amine, d-amphetamine, was inactive in the monoamine-depleted rats, indicating that no dopamine was available for release by d-amphetamine. The muscarinic receptor antagonist, scopolamine, alone did not alter locomotion, but produced marked stimulation when combined with SKF38393 but not with quinpirole. This stimulation was not affected by haloperidol. However, the scopolamine plus SKF38393-induced stimulation was partially blocked by SCH23390 or by a combination of haloperidol and SCH23390. The data indicate that clozapine, in rats depleted of their dopamine stores, exhibits properties consistent with those of a dopamine receptor agonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Why does clozapine stimulate the motor activity of reserpine-pretreated rats when combined with a dopamine D1 receptor agonist? 749 68

Meige syndrome, which has been presented in tardive syndromes, is a form of blepharospasm accompanied by oromandibular dystonia with manifestations over the face, jaw, and neck. A blepharospasm can be induced by antihistamines, dopaminomimetic or sympathomimetic drugs, or long-term exposure to dopamine antagonists. Atypical antipsychotics have less extrapyramidal side effects because of a weak dopamine D2 receptor binding affinity or a strong antagonistic effect to serotonin 5-HT2a receptor and have been known to cause less tardive dyskinesia than typical antipsychotics. Thus, in literature, atypical antipsychotics are recommended for the treatment of psychosis in cases of tardive dyskinesia. The potential risk factors associated with the development of tardive dyskinesia are extrapyramidal symptoms' history, diabetes mellitus, affective disorder, female gender, older age, and long-term therapy with neuroleptics at higher dosages. As reported below, a patient with an affective disorder who had quetiapine-induced oromandibular dystonia and olanzapine-induced Meige syndrome after antipsychotic augmentation in different stages of the disease process was presented.
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PMID:Tardive Blepharospasm and Meige Syndrome during Treatment with Quetiapine and Olanzapine. 2836 Jul 8