Evidence for selective and long-lasting stimulation of “regulatory” dopamine-receptors by bromocriptine (CB 154)

Chiara, G. Di; Porceddu, M.L.; Vargiu, L; Stefanini, E.; Gessa, Gian Luigi

doi:10.1007/bf00500966

Cited by 59 publications

(26 citation statements)

References 28 publications

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“…BRC produces a long lasting locomotor stimulation in mice, which is preceded by locomotor depression; these effects are considered to be the result of post-and pre-synaptic DA-receptor stimulation respectively (Johnson et aL, 1976;Fuxe et aL, 1978;Di Chiara et al, 1977;Snider et aL, 1976). We confirmed this result and noted that the stimulation could be substantially blocked by reserpine orAMPT and completely by both pretreatments together (Table 1).…”

Section: Resultssupporting

confidence: 89%

Hypothesis: Bromocriptine lacks intrinsic dopamine receptor stimulating properties

Jackson

Jenkins

1985

J. Neural Transmission

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Bromocriptine (BRC) produced neither locomotor stimulation nor stereotyped behavior in mice and rats pretreated with reserpine plus alpha-methyl-p-tyrosine (AMPT). However, the blockade of locomotor stimulation in mice by AMPT could be reversed by their prior treatment with a low, behaviorally inactive dose of L-DOPA. BRC potentiated the stereotypy (rats) and locomotor stimulation (mice) produced by apomorphine in animals pretreated with reserpine plus AMPT. Moreover, BRC potentiated the stimulant effect of d-amphetamine in reserpinized mice, while nomifensine, but not fluoxetine or desipramine, potentiated the stimulant effect of BRC in mice. After direct application to the nucleus accumbens or caudate nucleus of rats, BRC was inactive. However, when BRC and DA were applied together to the nucleus accumbens, BRC enhanced the stimulant effect of DA. These data show that BRC by itself does not cause behavioral stimulation in rodents. Despite having affinity for the DAD 2-receptor, BRC is incapable of causing excitation in rats and mice unless another DA-receptor agonist such as apomorphine or DA is present. The data are discussed in relation to the published literature and the hypothesis presented that BRC affects the signal transmitted by DA-receptor agonists such as apomorphine at or beyond the postsynaptic DA-receptor.

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Section: Resultssupporting

confidence: 89%

Hypothesis: Bromocriptine lacks intrinsic dopamine receptor stimulating properties

Jackson

Jenkins

1985

J. Neural Transmission

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“…The magnitude of the decrease observed in the striatum and the nucleus accumbens agrees with the previous data obtained in whole brain, brain areas or brain slices (Barton et al, 1987;Carlsson et al, 1974;Corrodi et al, 1972;Di Chiara et al, 1977;Dolphin et al, 1977;Goldstein et al, 1973;Gudelsky and Moore, 1976;Hoffmann et al, 1986;Jackson et al, 1990;Ponzio et al, 1981;Sarati et al, 1991;Snider et al, 1976;Tissari et al, 1983;Westfall et al, 1983) or striatum microdialysates of anesthetized rats (Brannan et al, 1993). For the frontal cortex, Fuxe et al (1978a) found a 30% reduction of dopamine synthesis after bromocriptine (3 mg/kg).…”

Section: Discussionsupporting

confidence: 87%

Differential regional and kinetics effects of piribedil and bromocriptine on dopamine metabolites: a brain microdialysis study in freely moving rats

Pagliari

Peyrin

Crambes

1995

J. Neural Transmission

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Brain microdialysis coupled to HPLC was applied to freely moving rats to investigate the regional kinetics of piribedil and bromocriptine on the extracellular levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in striatum, nucleus accumbens, and frontal cortex. Both D2 agonists (20 mg/kg i.p.) decreased DOPAC and HVA in the three brain regions. The responsiveness of frontal cortex to both compounds was greater than those previously reported with other dopaminergic drugs. Regional and temporal differences were observed under piribedil: DOPAC and HVA levels decreased more in the nucleus accumbens than in striatum or frontal cortex but increased over basal values from the 5th hour in the frontal cortex suggesting a late stimulatory effect of piribedil on dopamine synthesis in this area. Such regional effects differentiate piribedil from most other D2 agonists and could explain some behavioural and therapeutic actions possibly related to involvement of nucleus accumbens or/and frontal cortex.

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“…Apomorphine (AP, 1 -1.5 mg SC) has been reported to provide rapid, if transient improvement of psychotic symptoms in unmedicated schizophrenics (Corsini et al 1977a, b;DiChiara et al 1978;Smith et al 1977). We reported no significant improvement in psychotic symptoms after 0.75 mg AP in 22 unmedicated schizophrenic patients (Meltzer 1979).There is preclinical behavioral and biochemical evidence that bromocriptine, an ergot alkaloid, is a DA autoreceptor agonist (Snider et al 1976;DiChiara et al 1977 Bannon et al 1981;Haubrich and Pfleuger 1982). Thus, bromocriptine might be expected to have antipsychotic effects in humans at the proper dosage.…”

mentioning

confidence: 64%

“…There is preclinical behavioral and biochemical evidence that bromocriptine, an ergot alkaloid, is a DA autoreceptor agonist (Snider et al 1976;DiChiara et al 1977;Marek and Bannon et al 1981;Haubrich and Pfleuger 1982). Thus, bromocriptine might be expected to have antipsychotic effects in humans at the proper dosage.…”

mentioning

confidence: 95%

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

et al. 1983

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Bromocriptine (0.5-6.0 mg/day) was administered to seven unmedicated chronic schizophrenic and two schizoaffective patients. Transient slight improvement was noted in four patients and marked improvement in one other. Clinical improvement was associated with nausea and drowsiness. These doses of bromocriptine stimulated serum growth hormone and inhibited serum prolactin levels in some subjects. These results suggest that bromocriptine may stimulate dopamine autoreceptors and, through this mechanism, attenuate symptoms in a small proportion of psychiatric patients.

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Evidence for selective and long-lasting stimulation of “regulatory” dopamine-receptors by bromocriptine (CB 154)

Cited by 59 publications

References 28 publications

Hypothesis: Bromocriptine lacks intrinsic dopamine receptor stimulating properties

Hypothesis: Bromocriptine lacks intrinsic dopamine receptor stimulating properties

Differential regional and kinetics effects of piribedil and bromocriptine on dopamine metabolites: a brain microdialysis study in freely moving rats

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

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