Bromocriptine, an ergot-derivate with DA-receptor stimulating properties in vivo, produces long-lasting hypomotility in mice not accustomed to the motility cage and decreases brain DOPAC and HVA without affecting brain DA. These effects are obtained with doses 25 times lower than those which produce hypermotility. The decrease of brain DOPAC is correlated to the hypomotility both on a dose- and on a time-basis. Potent neuroleptics as pimozide, benzperidol and droperidol, which are considered to be fairly specific DA-receptor blockers, antagonize the hypomotility and the decrease of brain DOPAC produced by bromocriptine. These effects are obtained with very low doses (0.05--0.3 mg/kg) of neuroleptics which per se do not affect motility or brain DOPAC. The maximal decrease of brain DOPAC and HVA produced by bromocriptine is similar to that produced by apomorphine and the combination of these drugs does not result in a further decrease of brain DOPAC or HVA. On the basis of these results it is postulated that bromocriptine decreases brain DA-turnover and produces hypomotility by acting on "regulatory" DA-receptors different from the post-synaptic ones of the "terminal" dopaminergic areas.
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