Small doses of apomorphine and chronic administration of d-amphetamine reduce locomotor hyperactivity produced by radiofrequency lesions of dopaminergic A10 neurons area.
The lesion of the ventral mesencephalic tegmentum region (VMT) induces a behavioral syndrome characterized mainly by locomotor hyperactivity and reduction of attention processes. Previous data indicated that this syndrome was due at least in part to the destruction of dopaminergic (DA) A10 neurons. In order to test this hypothesis, we examined the effects of two dopaminomimetics drugs: apomorphine (APO) and d-amphetamine (d-AMPH) on the VMT behavioral syndrome. The acute administration of very low doses of APO (30 microgram/KG; Sc) reduces the behavioral deficits; similarly a chronic administration of d-aMPH (two injections daily for 43 days) reduces locomotor hyperactivity. In these two cases, the lesioned rats activity reaches the control level. These results confirm the primary role of DA-A10 neurons in the VMT behavioral syndrome. Acute APO and chronic d-AMPH effects are discussed in terms of (i) reactivation of DA postsynaptic receptors disafferented after DA-A10 group destruction and (ii) strengthening of the hyperfunctioning of the remaining DA-A10 neurons. VMT-A10 syndrome could be a good animal model for pathophysiological studies.
D000818:Animals; D001058:Apomorphine / Q000008:administration & dosage*; D003913:Dextroamphetamine / Q000008:administration & dosage*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D006948:Hyperkinesis / Q000188:drug therapy*; D008297:Male; D008959:Models, Neurological; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology*; D013681:Tegmentum Mesencephali / Q000503:physiopathology*
D011954:Receptors, Dopamine; D001058:Apomorphine; D003913:Dextroamphetamine