The motor effects of bromocriptine ? a review

Abstract

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.

Effect of coadministration of glutamate receptor antagonists and dopaminergic agonists on locomotion in monoamine-depleted rats

“…This could possibly be due to differences in the application regimen of bromocriptine (Svensson et al, 1992) or the use of dopamine D2 receptor agonists with different pharmacokinetic properties (Goodwin et al, 1992;Starr and Starr, 1994;Ferr6 et al, 1994). It is known that bromocriptine has unique pharmacodynamic properties, such as: modest antagonism at the dopamine D1 receptor (Coleman, 1992), the need for simultaneous D1 receptor activation to induce locomotion (Jackson et al, 1988), or its biphasic dose-response curve i.e. increase of striatal dopamine release at lower doses and a decrease at higher doses (Brannan et al, 1993).…”

NeurobiologicalMechanismsInvolved inSleepBruxism

“…Moreover, most neurochemical substances used so far have a cross-affinity with other receptor families. For example, bromocriptine presents a cross-affinity for DA and Adr receptors (Jackson et al, 1988), and propranolol for Adr and 5-HT receptors (Hindle, 1994). In addition, several neurochemical substances have been associated with RJM (Table 2), and in the absence of controlled studies, it is premature to associate these with SB pathophysiology.…”

The effect of chronic unpredictable stress on locomotor and exploratory activity in male rats with different endogenous prolactin levels

“…Interpretation of these findings is not simple. One possible argument is to assume that bromocriptine has an action in the central nervous system (Jackson et al, 1988). The dopamine agonist at the dose used in the present report (5 mg/kg) has been shown to stimulate locomotor activity (Jackson etal., 1988).…”