Electrolytic lesions of the substantia innominata and lateral preoptic area attenuate the 'supersensitive' locomotor response to apomorphine resulting from denervation of the nucleus accumbens.

Apomorphine-stimulated locomotion in the rat is greatly enhanced following destruction of dopamine terminals in the nucleus accumbens (NA) with 6-hydroxydopamine (6-OHDA). While this augmented response is ascribed to the action of the dopamine stimulant apomorphine on supersensitive receptors within the NA, little is known regarding the mechanisms by which increased receptor stimulation within the NA influences lower motor circuitry to produce changes in locomotion. In this study, we examined apomorphine-stimulated locomotion in 6-OHDA-infused rats following electrolytic damage to the terminal region of first-order NA efferent fibers within the substantia innominata and lateral preoptic area. This damage greatly diminished the locomotor response to apomorphine in 6-OHDA-infused animals, but did not diminish locomotion in vehicle-infused animals. Destruction of dopamine terminals within the NA has also been reported to enhance the place-preference response to apomorphine in rats. Damage to the substantia innominata and lateral preoptic area significantly decreased the place-preference for apomorphine-paired environments in 6-OHDA-infused animals, but did not alter place-preference responses in vehicle-infused animals. Our results indicate that the efferent pathway from the NA to the substantia innominata and lateral preoptic area serves as an important output of mesolimbic activity into motor circuitry involved in the expression of apomorphine-stimulated locomotion and place-preference.