Effects of lesions of the ventral medial tegmentum on locomotor activity, biogenic amines and responses to amphetamine in rats.

Rats subjected to electrolytic lesions of the ventral medial tegmentum (VMT) showed long-lasting increased locomotor activity in the open field compared to sham-operated controls. In addition to severe depletion of mesolimbic dopamine, the lesions also caused significant depletions of striatal dopamine, mesolimbic and striatal norepinephrine and striatal and hippocampal serotonin. Administration of d-amphetamine sulfate produced similar dose-response functions for locomotor activity in both VMT-lesioned and sham-operated rats despite the extensive depletion of dopamine in the VMT-lesioned rats. These results suggest that the mesolimbic dopamine pathway is not the sole substrate for amphetamine-stimulated locomotor activity. Electrolytic lesions of the VMT interrupt several neurotransmitter pathways which may produce complex and antagonistic effects on behavior.