Abstract
The effects of total (T-NSB) and subtotal (S-NSB) destruction of the nigrostriatal bundle (NSB) were compared with the effects of large lateral hypothalamic (LH) lesions on various aspects of the lateral hypothalamic syndrome. The T-NSB and LH lesions produced equivalent decreases in caudate and telencephalic contents of dopamine and norepinephrine, while with the exception of telencephalic dopamine, S-NSB lesions had consistently smaller effect. The T-NSB and LH lesions produced equivalent effects on duration of aphagia and adipsia (Stages 1-3) and on long-term decreases in body weight and ad lib water comsumption, and these effects were always greater than those produced by the S-NSB lesion. These aspects of the lateral hypothalamic syndrome appeared to be related to the interruption of the nigrostriatal bundle and consequent decrease in caudate dopamine. The T-NSB and S-NSB lesions produced equivalent long-term deficits in water regulation as measured by drinking in the absence of food or in response to intra- and extracellular dehydration, but these deficits were always significantly less than those produced by the LH lesion. These regulatory deficits were probably not related to destruction of catecholamine pathways. All 3 lesions totally blocked eating in response to a glucoprivic challenge. This aspect of the lateral hypothalamic syndrome results from destruction of a small portion of the lateral diencephalon and may be related to the interuption of the dopaminergic mesolimbic system.