Behavioural supersensitivity to apomorphine following cerebral dopaminergic denervation by 6-hydroxydopamine.
Intraventricular injections of 6-hydroxydopamine that induce a marked and long lasting depletion of cerebral dopamine as well as noradrenaline, greatly enhanced the stimulation of locomotor activity of mice produced by the injection of apomorphine. Dose-response relationships indicated that the maximal response to apomorphine was greatly increased but that there was no apparent change in the ED50 from the response in vehicle-treated mice. 6-Hydroxydopamine treated mice were also considerably less susceptible to the cataleptic activity of pimozide and it is suggested that cerebral dopaminergic denervation may result in an increased number of available post-synaptic dopamine receptors.
D001058:Apomorphine / Q000494:pharmacology*; D001923:Brain Chemistry / Q000187:drug effects; D002375:Catalepsy / Q000139:chemically induced; D004298:Dopamine / Q000032:analysis / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D006892:Hydroxydopamines / Q000494:pharmacology*; D007276:Injections, Intraventricular; D009043:Motor Activity / Q000187:drug effects* / Q000502:physiology; D009638:Norepinephrine / Q000032:analysis; D010868:Pimozide / Q000494:pharmacology; D011955:Receptors, Drug / Q000187:drug effects; D013268:Stimulation, Chemical; D013562:Sympathectomy
D006892:Hydroxydopamines; D011955:Receptors, Drug; D010868:Pimozide; D001058:Apomorphine; D004298:Dopamine; D009638:Norepinephrine