Contributions of the mesencephalic dopaminergic system and the trigeminal sensory pathway to the ventral tegmental aphagia syndrome in rats

Abstract

Four experiments examined the neural substrates for the aphagia and adipsia syndrome resulting from damage of the ventral tegmental region. Radiofrequency (RF) lesions at the level of the mesencephalon in rats showed that the most effective site for producing aphagia and adipsia was in an intermediate zone between the substantia nigra and the ventral tegmental area. Injection of the neurotoxin 6-hydroxydopamine (6-OHDA) into this intermediate zone led to a less severe feeding deficit, suggesting that both dopaminergic and non-dopaminergic neurons are involved in the mesencephalic aphagic syndrome. As the lemniscus trigeminalis was destroyed after the RF lesion of the intermediate zone, the hypothesis of trigeminal projection involvement was tested by lesioning (RF) the sensory trigeminal nucleus. These rats were aphagic but they recovered and their deficit was less severe than after RF lesion of the mesencephalic intermediate zone. In the last experiment, a combined 6-OHDA lesion of the mesencephalic intermediate zone and RF lesion of the trigeminal sensory nucleus led to a more severe deficit in feeding behavior than either lesion alone. These results further demonstrate that feeding behavior is under the control of a complex system involving several neural pathways.