title: Effects of intralaminar thalamic nuclei lesion on glutamic acid decarboxylase (GAD65 and GAD67) and cytochrome oxidase subunit I mRNA expression in the basal ganglia of the rat.
abstract: This study investigated the influence of thalamic inputs on neuronal metabolic activity in the rat basal ganglia. By means of in situ hybridization histochemistry, we examined the consequences of ibotenate-induced unilateral lesion of intralaminar thalamic nuclei on mRNA expression of cytochrome oxidase subunit-I (CoI) in the striatum and the subthalamic nucleus (STN) and of the two isoforms of glutamate decarboxylase (GAD65 and GAD67) in the striatum, globus pallidus (GP), entopeduncular nucleus (EP) and substantia nigra pars reticulata (SNr). In the striatum, GAD67 mRNA expression decreased selectively in the rostral part of the structure at 5 and 12 days postlesion (approximately -30%), whereas, GAD65 mRNA levels was downregulated only in the caudal striatum at 12 days (-29%). In both the striatum and STN, CoI mRNA expression decreased ipsilaterally at 5 and bilaterally at 12 days. In GP, GAD67 and GAD65 mRNA expression decreased ipsilaterally at 5 (-20% and -26%) and 12 days (-23% and -36%). In EP, selective bilateral decreases in GAD67 mRNA expression were found at 5 and 12 days (-50% and -40%). Conversely, in SNr, only GAD65 mRNA expression was reduced bilaterally at both time points. These data show that the thalamus exerts a widespread excitatory influence on the basal ganglia network that cannot be accounted for solely by its known direct connections. Given the recent data showing that intralaminar thalamic nuclei are a major nondopaminergic site of neurodegeneration in Parkinson's disease, these results may have a critical bearing on understanding the cellular basis of basal ganglia dysfunction in parkinsonism.
authors.affiliation: Laboratoire de Neurobiologie Cellulaire et Fonctionnelle, UPR 9013, CNRS, 31 chemin Joseph Aiguier, 13 402 Marseille Cedex 20, France.
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Bacci
authors.forename: Lydia
authors.initials: L
authors.lastname: Kerkerian-Le Goff
authors.forename: Pascal
authors.initials: P
authors.lastname: Salin
mesh_terms: D000818:Animals; D001479:Basal Ganglia / Q000201:enzymology* / Q000503:physiopathology; D003714:Denervation; D015536:Down-Regulation / Q000502:physiology; D003576:Electron Transport Complex IV / Q000235:genetics*; D020392:Entopeduncular Nucleus / Q000201:enzymology / Q000503:physiopathology; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D005917:Globus Pallidus / Q000201:enzymology / Q000503:physiopathology; D005968:Glutamate Decarboxylase / Q000235:genetics*; D020646:Intralaminar Thalamic Nuclei / Q000201:enzymology* / Q000293:injuries / Q000503:physiopathology; D007527:Isoenzymes / Q000235:genetics*; D017072:Neostriatum / Q000201:enzymology / Q000503:physiopathology; D009434:Neural Pathways / Q000201:enzymology* / Q000503:physiopathology; D010300:Parkinson Disease / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013378:Substantia Nigra / Q000201:enzymology / Q000503:physiopathology; D020531:Subthalamic Nucleus / Q000201:enzymology / Q000503:physiopathology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D007527:Isoenzymes; D012333:RNA, Messenger; D005680:gamma-Aminobutyric Acid; D003576:Electron Transport Complex IV; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; C401141:glutamate decarboxylase 2