title: Modifications of local cerebral glucose utilization in thalamic structures following injection of a dopaminergic agonist in the nucleus accumbens--involvement in antiepileptic effects?
abstract: Dopaminergic transmission in the nucleus accumbens (NAcc) is implicated in different aspects of reward and motivational mechanisms. More recently, it has been suggested that this nucleus could also be involved in the modulation of generalized epileptic seizures. In particular, microinjection of dopaminergic agonists in the NAcc suppresses the occurrence of epileptic seizures in a model of absence seizures, the GAERS (generalized absence epileptic rats from Strasbourg). The aim of this study was to identify the structures involved in this effect. Local cerebral metabolic rates for glucose utilization (LCMRglc) were measured in different parts of the basal ganglia and output structures after apomorphine injection in the NAcc in GAERS and in the inbred non-epileptic rats (NE), concomitantly with seizure suppression. Apomorphine injection in the NAcc induced a significant increase of glucose intake in the anteromedial, mediodorsal and ventrolateral nuclei of the thalamus in NE rats, while no significant changes were observed in the basal ganglia structures (globus pallidus, subthalamic nucleus, substantia nigra). Furthermore, microinjections of muscimol (100 and 200 pmol/side) in the mediodorsal nucleus of the thalamus in GAERS rats suppressed seizures. These results suggest that the mediodorsal nucleus of the thalamus could be involved in absence seizures modulation. Along with data from the literature, our data suggest that this nucleus could participate in the control of the basal ganglia over generalized epileptic seizures.
authors.affiliation: Neurobiologie et Neuropharmacologie des Epilepsies Généralisées, INSERM U. 398, Faculté de Médecine, F-67085 Strasbourg Cedex, France. vriban@ucla.edu
authors.forename: V
authors.initials: V
authors.lastname: Riban
authors.forename: A
authors.initials: A
authors.lastname: Pereira de Vasconcelos
authors.forename: B T
authors.initials: BT
authors.lastname: Phâm-Lê
authors.forename: A
authors.initials: A
authors.lastname: Ferrandon
authors.forename: C
authors.initials: C
authors.lastname: Marescaux
authors.forename: A
authors.initials: A
authors.lastname: Nehlig
authors.forename: A
authors.initials: A
authors.lastname: Depaulis
mesh_terms: D000818:Animals; D001058:Apomorphine / Q000494:pharmacology / Q000627:therapeutic use; D001345:Autoradiography; D001479:Basal Ganglia / Q000187:drug effects / Q000378:metabolism; D003847:Deoxyglucose / Q000493:pharmacokinetics; D004195:Disease Models, Animal; D018491:Dopamine Agonists / Q000494:pharmacology* / Q000627:therapeutic use; D004569:Electroencephalography / Q000187:drug effects; D004832:Epilepsy, Absence / Q000188:drug therapy* / Q000378:metabolism*; D018755:GABA Agonists / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D008297:Male; D008845:Microinjections; D009118:Muscimol / Q000494:pharmacology; D009714:Nucleus Accumbens / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D017208:Rats, Wistar; D013787:Thalamic Nuclei / Q000187:drug effects / Q000378:metabolism; D013788:Thalamus / Q000187:drug effects / Q000378:metabolism*
chemical_list: D018491:Dopamine Agonists; D018755:GABA Agonists; D009118:Muscimol; D003847:Deoxyglucose; D005947:Glucose; D001058:Apomorphine