title: Effect of neurotoxic lesion of pedunculopontine nucleus in nigral and striatal redox balance and motor performance in rats.
abstract: Early degeneration of pedunculopontine nucleus (PPN) is considered part of changes that characterize premotor stages of Parkinson's disease (PD). In this paper, the effects of unilateral neurotoxic lesion of the PPN in motor execution and in the development of oxidative stress events in striatal and nigral tissues in rats were evaluated. The motor performance was assessed using the beam test (BT) and the cylinder test (CT). Nigral and striatal redox balance, was studied by means of biochemical indicators such as malondialdehyde (MDA), nitric oxide (NO) and the catalase enzymatic activity (CAT EA). Lesioned rats showed fine motor dysfunction expressed both as an increase in the length (p<0.001) and deviation (p<0.001) of the traveled path and also in the time spent (p<0.01) in the circular small beam (CBS) (p<0.01) in comparison with control groups. In addition, the lesioned rats group presented a right asymmetry index greater than 0.5 which is consistent with a significant increase in the percentage of use of the right forelimb (ipsilateral to the lesion), compared with the control group (p<0.05). Biochemical studies revealed that after 48-h PPN neurotoxic injury, the CAT EA showed a significant increase in the subtantia nigra pars compacta (SNpc) (p<0.05). This significant increase of CAT EA persisted in the nigral tissue (p<0.001) and reached the striatal tissue (p<0.001) seven days after PPN injury. Also at seven days post-injury PPN, increased concentrations of MDA (p<0.01) and a tendency to decrease in the concentrations of NO in both structures (SNpc and striatum) were found. The events associated with the generation of free radicals at nigral and striatal levels, can be part of the physiological mechanisms underlying motor dysfunction in rats with unilateral PPN neurotoxic lesion.
authors.affiliation: Experimental Neurophysiology Department, International Center of Neurological Restoration, Avenue 25 No. 15805 e/ 158 and 160. Playa, Havana CP 11300, Cuba; Neuro Investigation Department, Cuban Neuroscience Center, 190th Street e/ Ave. 25 and Avenue 27. Playa, Havana CP 11300, Cuba.
authors.forename: J
authors.initials: J
authors.lastname: Jimenez-Martin
authors.affiliation: Experimental Neurophysiology Department, International Center of Neurological Restoration, Avenue 25 No. 15805 e/ 158 and 160. Playa, Havana CP 11300, Cuba; Faculty of Sciences, Tolima University, 42nd Street, Barrio Santa Elena, Parte Alta, CP 730001, Colombia. Electronic address: lisette.blanco@infomed.sld.cu.
authors.forename: L
authors.initials: L
authors.lastname: Blanco-Lezcano
authors.affiliation: Experimental Neurophysiology Department, International Center of Neurological Restoration, Avenue 25 No. 15805 e/ 158 and 160. Playa, Havana CP 11300, Cuba.
authors.forename: M E
authors.initials: ME
authors.lastname: González-Fraguela
authors.affiliation: Experimental Neurophysiology Department, International Center of Neurological Restoration, Avenue 25 No. 15805 e/ 158 and 160. Playa, Havana CP 11300, Cuba.
authors.forename: M-L
authors.initials: ML
authors.lastname: Díaz-Hung
authors.affiliation: Experimental Neurophysiology Department, International Center of Neurological Restoration, Avenue 25 No. 15805 e/ 158 and 160. Playa, Havana CP 11300, Cuba.
authors.forename: T
authors.initials: T
authors.lastname: Serrano-Sánchez
authors.affiliation: Neuro Investigation Department, Cuban Neuroscience Center, 190th Street e/ Ave. 25 and Avenue 27. Playa, Havana CP 11300, Cuba.
authors.forename: J L
authors.initials: JL
authors.lastname: Almenares
authors.affiliation: Faculty of Sciences, Tolima University, 42nd Street, Barrio Santa Elena, Parte Alta, CP 730001, Colombia; Experimental Neurophysiology Department, International Center of Neurological Restoration, Avenue 25 No. 15805 e/ 158 and 160. Playa, Havana CP 11300, Cuba.
authors.forename: L
authors.initials: L
authors.lastname: Francis-Turner
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D003342:Corpus Striatum / Q000502:physiology*; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005552:Forelimb / Q000503:physiopathology; D007839:Functional Laterality; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009043:Motor Activity / Q000502:physiology*; D009069:Movement Disorders / Q000503:physiopathology; D016202:N-Methylaspartate / Q000633:toxicity; D009569:Nitric Oxide / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D045042:Pedunculopontine Tegmental Nucleus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D004856:Postural Balance / Q000502:physiology*; D017208:Rats, Wistar; D013378:Substantia Nigra / Q000502:physiology*
chemical_list: D018690:Excitatory Amino Acid Agonists; D009569:Nitric Oxide; D008315:Malondialdehyde; D016202:N-Methylaspartate; D002374:Catalase
keywords: oxidative stress; pedunculopontine nucleus; striatum; substantia nigra compacta