Effect of low-dose bromocriptine in treatment of psychosis: The dopamine autoreceptor-stimulation strategy

Meltzer, Herbert Y.; Kołakowska, T; Robertson, Alan; Tricou, Betty Jo

doi:10.1007/bf00439271

Cited by 43 publications

(14 citation statements)

References 29 publications

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“…As expected (Bowers et al 1984, Gruen et al 1978, Meltzer and Fang 1976, Meltzer et al 1983, Minderaa et al 1989, Smith et al 1980), amisulpride and bromocriptine had opposite effects on plasma prolactin (p < 0.01).…”

Section: Plasma Prolactinsupporting

confidence: 54%

Catecholamines in Autistic Disorder: Effects of Amisulpride and Bromocriptine in a Controlled Crossover Study

Dollfus¹,

Petit²,

Garnier³

et al. 1993

Journal of Child and Adolescent Psychopharmacology

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The biochemical effects on catecholaminergic systems of the dopamine antagonist amisulpride and the dopamine agonist bromocriptine were evaluated in a double-blind, randomized, crossover study in children with autistic disorder. Plasma levels of dopamine, norepinephrine, and epinephrine; urinary concentrations of homovanillic acid (HVA), vanillyImandelic acid (VMA) and 3-methoxy-4-hydroxyphenylethylene glycol (MHPG); and plasma prolactin were measured. At doses of amisulpride and bromocriptine that had the expected opposing effects on plasma prolactin, the drugs' effects on the catecholaminergic systems were similar. Both agents unexpectedly lowered urinary HVA (total, free, and sulfated) although only amisulpride decreased the HVA levels significantly. This paradoxical decrease in HVA levels suggests that both dopamine agonists and antagonists could act on autoreceptors or presynaptic dopaminergic receptors in the central nervous system. There was no significant action of either drug on plasma epinephrine, urinary VMA, or urinary MHPG, suggesting that neither drug altered norepinephrine or epinephrine systems; however, a weak increase of plasma norepinephrine occurred after amisulpride treatment, consistent with effects observed with other neuroleptics. Neither agent altered plasma dopamine, suggesting that peripheral dopamine metabolism was unchanged. The clinical effects of amisulpride and bromocriptine have been reported to be unexpectedly complementary. The complementary clinical effects of a dopamine agonist and dopamine antagonist might speculatively be related to their similar action on dopamine autoreceptors, leading to a correction of the dopaminergic hyperactivity that has been postulated in autistic children.

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Section: Plasma Prolactinsupporting

confidence: 54%

Catecholamines in Autistic Disorder: Effects of Amisulpride and Bromocriptine in a Controlled Crossover Study

Dollfus¹,

Petit²,

Garnier³

et al. 1993

Journal of Child and Adolescent Psychopharmacology

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show abstract

“…1977;Tamminga et al 1978;Meltzer et al 1983;Cutler et al 1984) and Gille delaTourette's disease (Feinberg and Carroll 1979) as well as neurological disorders such as Huntington's chorea, tardive dyskinesia and torticollis (Tolosa and Spar- Carroll et al 1977;Tolosa 1978). Later reports have been less optimistic, showing that the effects on schizophrenia are shortlived and prone to desensitization Tamminga and Shaffer 1979;Hollister et al 1980;Hollister 1981;Tamminga et al 1986).…”

Section: Discussionmentioning

confidence: 90%

Do autoreceptors mediate dopamine agonist — induced yawning and suppression of exploration? A critical review

Ståhle

1992

Psychopharmacology

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The hypothesis that stimulation of dopamine autoreceptors is the mechanism by which dopamine agonists induce yawning and suppression of exploration is critically examined. It is shown that the relation between reduced extracellular dopamine levels, assessed by microdialysis, and behavioural effects of dopamine agonists, a dopamine synthesis inhibitor and a granule storage blocker is highly inconsistent. The time-course and duration of the behavioural effects of dopamine agonists differ from the reduction of extracellular dopamine. Amphetamine cotreatment is shown to increase dopamine levels, while yawning and suppression of exploration can still be induced. The data strongly indicate that autoreceptors are not the mediators of these behavioural effects. It is proposed that postsynaptic receptors mediate dopamine agonist induced yawning and suppression of exploration. Evidence is also presented showing that yawning and suppression of exploration are not functionally equivalent.

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“…Due to its higher affinity for the presynaptic autoreceptor, it has been proposed to have an inhibitory effect on dopamine function at lower doses, whereas at higher doses its effects at the postsynaptic receptor are thought to predominate, resulting in a facilitatory effect on the dopaminergic system (Meltzer et al , 1983; Luciana and Collins, 1997). …”

Section: Catecholaminergic Therapiesmentioning

confidence: 99%

Catecholamines and cognition after traumatic brain injury

Jenkins

Mehta

Sharp

2016

Brain

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Effect of low-dose bromocriptine in treatment of psychosis: The dopamine autoreceptor-stimulation strategy

Cited by 43 publications

References 29 publications

Catecholamines in Autistic Disorder: Effects of Amisulpride and Bromocriptine in a Controlled Crossover Study

Catecholamines in Autistic Disorder: Effects of Amisulpride and Bromocriptine in a Controlled Crossover Study

Do autoreceptors mediate dopamine agonist — induced yawning and suppression of exploration? A critical review

Catecholamines and cognition after traumatic brain injury

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