title: [Glucose metabolism in the basal ganglia].
abstract: GABAergic neurons in the substantia nigra pars reticulata (SNr) -a major output nucleus of the basal ganglia- are involved in sensing severe hypoglycemic and hypoxic conditions in the brain via the ATP-sensitive potassium (KATP) channels that are abundantly expressed in these neurons. However, these neurons are also sensitive to mild changes in extracellular glucose concentrations through KATP channel-independent, yet unknown mechanisms. Lenard et al. reported that globus pallidus (GP) -another output nucleus of the basal ganglia- also senses glucose concentrations in the brain. It is unclear why these two major output nuclei sense glucose concentrations. It has been reported that some SNr and GP neurons respond to feeding-related, jaw or hand movement. Interestingly, Nishino demonstrated that SNr neurons responded oppositely, i.e., increased or decreased in their firings, to the same sweet food depending on blood glucose levels. Thus, glucose levels might influence feeding-related information processing in the basal ganglia through SNr and GP. Other issues reviewed are regarding associations between glucose metabolism and motor diseases in the basal ganglia. These include mutation in glucose transporter (GLUT) 1 causing paroxysmal kinesigenic choreoarthetosis, abnormal glycolysis in Huntington's disease, and a study showing increased glucose metabolism in SNr and GP in Parkinson's disease using high-resolution research positron emission tomography (HRRT). Although glucose is the sole energy source for the brain, its utilization at the single-cell level remains elusive. Modern methods for investigating intercellular metabolic communication might help understanding the selective vulnerability seen in the basal ganglia of patients suffering from such neurodegenerative disorders in near future.
authors.affiliation: Department of Physiology, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki-shi, Aomori 036-8562, Japan.
authors.forename: Katsuya
authors.initials: K
authors.lastname: Yamada
mesh_terms: D001479:Basal Ganglia / Q000378:metabolism*; D003342:Corpus Striatum / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D002149:Energy Intake; D005917:Globus Pallidus / Q000502:physiology; D005947:Glucose / Q000378:metabolism*; D051272:Glucose Transporter Type 1 / Q000235:genetics / Q000502:physiology; D006801:Humans; D009154:Mutation; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000378:metabolism; D009474:Neurons / Q000502:physiology; D013378:Substantia Nigra / Q000502:physiology
chemical_list: D051272:Glucose Transporter Type 1; D005947:Glucose; D004298:Dopamine