Microelectrophoretic studies with 2-bromo-α-ergocriptine on dopaminergic neurons in the feline caudate nucleus

Gmelin, Gernot W.

doi:10.1016/0024-3205(78)90158-3

Cited by 10 publications

(1 citation statement)

References 3 publications

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“…If bromocriptine is applied iontophoretically to ventral tegmental area cells, their activity is suppressed; this action is blocked by sulpiride but not by SCH23390 (White and Wang 1984). Gmelin (1978) noted that the effects of bromocriptine on cat caudate nucleus DA cells, mediated through D2 receptors (Ohno et al 1986), were similar to those of DA, with the activity of one type being inhibited and the other type being excited by both DA and bromocriptine. Interestingly, the iontophoretic application of bromocriptine enhanced the effect of DA on cells which were inhibited by DA, even though bromocriptine itself was without significant effect (Table 3).…”

Section: Studies Of the Presynaptie Effects Of Bromocripfinementioning

confidence: 99%

The motor effects of bromocriptine ? a review

1988

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For many years, bromocriptine has proven to be a useful treatment for some of the disabling motor effects seen in Parkinson's disease. As such, it has been the only commonly used directly acting D2 agonist available. But its mechanism of action has been obscure because many animal models indicated an absolute requirement for the presence of endogenous DA for bromocriptine to have any efficacy, despite its undoubted occupation of the D2 receptor with high affinity. Several scattered reports indicated, however, that bromocriptine could potentiate the effects of a number of other dopamine agonists (such as apomorphine and L-dopa) in a variety of pharmacological models and in the clinic. With the availability of SKF38393 and SCH23390, it soon became clear that bromocriptine, while a selective D2 agonist, depended in an absolute sense on the integrity of the D1 receptors. Thus, if SKF38393 was administered together with bromocriptine to rodents depleted of dopamine, marked locomotor excitation was produced, despite either drug alone being inactive. The present review explores the literature on the motor effects of bromocriptine and endeavours to integrate its behavioural, biochemical and electrophysiological effects into a coherent whole. It closes with a consideration of several remaining unsolved problems associated with the pharmacology of bromocriptine and suggests some future studies.

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Section: Studies Of the Presynaptie Effects Of Bromocripfinementioning

confidence: 99%

The motor effects of bromocriptine ? a review

1988

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Bromocriptine potentiates the behavioural effects of directly and indirectly acting dopamine receptor agonists in mice

Jenkins

Jackson

1985

Naunyn-Schmiedeberg's Arch. Pharmacol.

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After an initial period of depression which lasted up to 90 min following injection, bromocriptine (BRC, 5-20 mg/kg, IP) produced dose-dependent and long lasting (7 h) locomotor stimulation in mice. The locomotor stimulation was antagonised by reserpine, alpha-methyl-p-tyrosine (AMPT) or haloperidol. The blockade by AMPT of BRC's locomotor stimulant effect was reversed by prior treatment of the mice with a low, behaviourally inactive dose of L-Dopa plus benserazide. In mice pretreated with reserpine, BRC enhanced the stimulant action of d-amphetamine. Moreover, in mice pretreated with reserpine plus AMPT, BRC significantly enhanced the locomotor stimulant effect of apomorphine. This ability of BRC to enhance the effect of apomorphine commenced as soon as 20 min after BRC administration and lasted for at least 8 h. The dopamine (DA) uptake inhibitor and DA receptor agonist nomifensine potentiated and prolonged the stimulant effect of BRC while inhibitors of the neuronal uptake of noradrenaline (desipramine) and 5-hydroxytryptamine (fluoxetine) were without marked effect. The results clearly show that BRC, in behavioural terms, has no efficacy per se at the postsynaptic DA receptor and that it requires either DA or the administration of an exogenous agonist such as apomorphine for the expression of its effects.

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Bromocriptine-induced locomotor stimulation in mice is modulated by dopamine D-1 receptors

Jackson

Hashizume

1987

J. Neural Transmission

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Mice were pretreated with reserpine plus alpha-methyl-p-tyrosine (10 mg/kg plus 200 mg/kg). One hour later they were administered the selective dopamine D-2 agonist bromocriptine or vehicle. Three hours after the bromocriptine, mice were challenged with the selective D-1 agonist SKF 38393, and locomotor activity was measured each 5 min for three hours. Neither bromocriptine nor SKF 38393 produced significant stimulation. The combination, however, produced a dose-dependent and coordinated increase in activity. If the bromocriptine was given only one hour before the SKF 38393 challenge (i.e., three hours after the reserpine plus alpha-methyl-p-tyrosine), no interaction was seen. In naive mice, when SKF 38393 and bromocriptine were administered together, the locomotor response to bromocriptine was quantitatively and qualitatively altered. The initial depressant response to bromocriptine was shortened, producing a more rapid onset of the stimulant response. In one experiment, the maximal activity induced by bromocriptine was increased by SKF 38393. The ability of SKF 38393 to alter the locomotor stimulant effect of bromocriptine in naive mice was blocked by their pretreatment with the selective D-1 antagonist, SCH 23390. The data indicate that the locomotor stimulant effects of bromocriptine are modulated by D1 receptors.

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Microelectrophoretic studies with 2-bromo-α-ergocriptine on dopaminergic neurons in the feline caudate nucleus

Cited by 10 publications

References 3 publications

The motor effects of bromocriptine ? a review

The motor effects of bromocriptine ? a review

Bromocriptine potentiates the behavioural effects of directly and indirectly acting dopamine receptor agonists in mice

Bromocriptine-induced locomotor stimulation in mice is modulated by dopamine D-1 receptors

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