title: A role for the dopaminergic nigrostriatal bundle in the pathogenesis of altered brain glucose consumption after lateral hypothalamic lesions. Evidence using the 14C-labeled deoxyglucose technique.
abstract: The pattern of altered brain glucose consumption which results from unilateral electrolytic lesions of the lateral hypothalamic area in albino rats is first described. Glucose consumption was estimated using the 2-deoxy-D-[14C]glucose tracer technique, which allows for the in vivo determination of the rates of glucose consumption of individual structures within the brain. Unilateral lesions resulted in a decrease of the glucose consumption of a number of structures rostral and ipsilateral to the lesion compared with that of the corresponding structures on the contralateral side. The lesion-associated depression of glucose consumption was greatest in sulcal prefrontal cortex, frontal cortex, parietal cortex, and caudatoputamen. No structure caudal to the lesion was affected. The deficit appeared acutely (2 h postoperatively) and persisted virtually unchanged for at least 14 days after the lesions had been made. Unilateral 6-hydroxydopamine lesions of the substantia nigra resulted in a decrease of the glucose consumption of a few of the ipsilateral structures which had been affected after the lateral hypothalamic lesions, most significantly in the ipsilateral caudatoputamen. In addition, the decreased glucose consumption of the ipsilateral caudatoputamen which had occurred after the lateral hypothalamic lesions disappeared when 1 mg/kg apomorphine hydrochloride was intravenously administered to the lesioned animals 14 days postoperatively. Thus, the decrease of ipsilateral caudatoputamen glucose consumption observed after unilateral electrolytic lateral hypothalamic lesions was (1) reproduced by 6-hydroxydopamine lesions of the substantia nigra and (2) reversed by intravenous apomorphine. Destruction of the ascending dopaminergic nigrostriatal bundle at the level of the lateral hypothalamus may have accounted for the reduced caudatoputamen glucose consumption which had been observed after lateral hypothalamic lesions.
authors.affiliation: Laboratory of Neurophysiology, National Institute of Mental Health, Bethesda, MD 20014, USA.
authors.forename: W J
authors.initials: WJ
authors.lastname: Schwartz
mesh_terms: D000818:Animals; D000963:Antimetabolites / Q000493:pharmacokinetics; D001345:Autoradiography; D002247:Carbon Isotopes / Q000493:pharmacokinetics; D003342:Corpus Striatum / Q000502:physiology*; D003847:Deoxyglucose / Q000493:pharmacokinetics; D004298:Dopamine / Q000378:metabolism*; D004572:Electrolysis / Q000379:methods; D005260:Female; D007839:Functional Laterality; D005947:Glucose / Q000378:metabolism*; D007026:Hypothalamic Area, Lateral / Q000293:injuries* / Q000378:metabolism*; D007930:Leucine / Q000493:pharmacokinetics; D009434:Neural Pathways / Q000502:physiology; D016627:Oxidopamine / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000293:injuries / Q000502:physiology*; D013565:Sympatholytics / Q000633:toxicity
chemical_list: D000963:Antimetabolites; D002247:Carbon Isotopes; D013565:Sympatholytics; D016627:Oxidopamine; D003847:Deoxyglucose; D007930:Leucine; D005947:Glucose; D004298:Dopamine