title: [The effects of lesions in the compact part of the substantia nigra on glutamate and GABA release in the pedunculopontine nucleus].
abstract: BACKGROUND
  The pedunculopontine nucleus (PPN), co-localized with the mesencephalic locomotor region, has been proposed as a key structure in the physiopathology of Parkinson's disease.
  
  
  OBJECTIVE
  The goal of the present study was to assess if the aminoacid neurotransmitter release in the PPN is modified by the degeneration of dopaminergic cells, from substantia nigra pars compacta in 6-hydroxidopamine (6-OHDA)-lesioned rats. In addition, it was studied the aminoacid neurotransmitter release in the PPN of rats with lesion of the subthalamic nucleus by quinolinic acid (QUIN) (100 nmol) intracerebral injection.
  
  
  METHODS
  Rats were assigned to five groups: untreated rats (I) (n = 13), 6-OHDA lesion (II) (n = 11), 6-OHDA + QUIN lesion (III) (n = 9), sham-operated (IV) (n = 10), QUIN, STN (V) lesioned (n = 9). The extracellular concentrations of glutamic acid (GLU) and gamma-aminobutyric acid (GABA) were determined by brain microdialysis and high performance liquid chromatography (HPLC). RESULTS. GLU released in PPN from 6-OHDA lesioned rats (group II), was significantly increased in comparison with the others groups (F(4, 47) = 18.21, p < 0.001). GABA released shows significant differences between experimental groups (F(4, 45) = 12.75, p < 0.001). It was detected a higher valour (p < 0.05) in-group II. The groups III and IV exhibited intermeddle valour (p < 0.001) and groups I and IV (p < 0.001) showed the lower GABA extracellular concentrations. The infusion of artificial cerebrospinal fluid with higher potassium (100 mmol) induced an increase in the GLU and GABA released in all groups, which confirm the neuronal origin of the extracellular content.
  
  
  CONCLUSIONS
  These results are in agreement with the current model of basal ganglia functioning and suggest the role of STN-PPN projection in the physiopathology of Parkinson's disease.
authors.affiliation: Departamento de Neurofisiología Experimental, Centro Internacional de Restauración Neurológica, Ciudad de la Habana, Cuba. lisette.blanco@infomed.sld.cu
authors.forename: L
authors.initials: L
authors.lastname: Blanco-Lezcano
authors.forename: L L
authors.initials: LL
authors.lastname: Rocha-Arrieta
authors.forename: L
authors.initials: L
authors.lastname: Alvarez-González
authors.forename: L
authors.initials: L
authors.lastname: Martínez-Martí
authors.forename: N
authors.initials: N
authors.lastname: Pavón-Fuentes
authors.forename: M E
authors.initials: ME
authors.lastname: González-Fraguela
authors.forename: Y
authors.initials: Y
authors.lastname: Bauzá-Calderín
authors.forename: Y
authors.initials: Y
authors.lastname: Coro-Grave de Peralta
mesh_terms: D018663:Adrenergic Agents / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D001923:Brain Chemistry; D004298:Dopamine / Q000378:metabolism; D018698:Glutamic Acid / Q000737:chemistry / Q000378:metabolism*; D008297:Male; D017551:Microdialysis; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D016627:Oxidopamine / Q000494:pharmacology; D010300:Parkinson Disease / Q000378:metabolism / Q000503:physiopathology; D045042:Pedunculopontine Tegmental Nucleus / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013378:Substantia Nigra / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005680:gamma-Aminobutyric Acid / Q000737:chemistry / Q000378:metabolism*
chemical_list: D018663:Adrenergic Agents; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D016627:Oxidopamine; D004298:Dopamine