Paradoxical Sleep Deprivation Modulates Tyrosine Hydroxylase Expression in the Nigrostriatal Pathway and Attenuates Motor Deficits Induced by Dopaminergic Depletion

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dc.contributor.author Lima, Marcelo M. S.
dc.contributor.author Andersen, Monica Levy [UNIFESP]
dc.contributor.author Reksidler, Angela B.
dc.contributor.author Ferraz, Anete C.
dc.contributor.author Vital, Maria Aparecida Barbato Frazão [UNIFESP]
dc.contributor.author Tufik, Sergio [UNIFESP]
dc.date.accessioned 2018-06-15T17:05:06Z
dc.date.available 2018-06-15T17:05:06Z
dc.date.issued 2012-06-01
dc.identifier https://dx.doi.org/10.2174/187152712800792839
dc.identifier.citation Cns & Neurological Disorders-drug Targets. Sharjah: Bentham Science Publ Ltd, v. 11, n. 4, p. 359-368, 2012.
dc.identifier.issn 1871-5273
dc.identifier.uri http://repositorio.unifesp.br/11600/43395
dc.description.abstract The nigrostriatal pathway is very likely involved in sleep regulation, considering the occurrence and high prevalence of sleep-related disorders in patients with Parkinson's disease. Indeed, dopaminergic neurons in the ventral tegmental area were recently shown to fire in bursts during paradoxical sleep (PS), but little is known about the activity of the nigrostriatal dopamine (DA) cells in relation to PS. In view of that we hypothesized that paradoxical sleep deprivation (PSD) may play a relevant role in nigrostriatal tyrosine hydroxylase (TH) expression and, subsequently, in sleep rebound. The present study was designed to determine the effects of PSD in the nigrostriatal pathway in mice by means of neurochemical and behavioral approaches. Intraperitoneal reserpine (1 mg/kg) associated to alpha-methyl-p-tyrosine (MT) (250 mg/kg) to produce catecholamine depletion, or rotenone (10 mg/kg) to increase striatal DA turnover were injected 30 min before the 24 h of PSD. Catalepsy and open-field tests indicated that motor deficits induced by reserpine-MT were counteracted by PSD, which, in contrast, potentiated the motor impairment induced by rotenone. Besides, PSD produced down-regulation on TH expression within the substantia nigra pars compacta and striatum, without affecting the number or the optical density of dopaminergic neurons present in the respective areas. Interestingly, PSD potentiated the down-regulation of TH expression in the substantia nigra pars compacta and striatum induced by the co-administration of reserpine-MT. These results reinforce the notion of a strong participation of DA in PS, as a consequence of the modulation of TH protein expression in the nigrostriatal pathway.. en
dc.description.sponsorship AFIP
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 359-368
dc.language.iso eng
dc.publisher Bentham Science Publ Ltd
dc.relation.ispartof Cns & Neurological Disorders-drug Targets
dc.rights Acesso restrito
dc.subject alpha-methyl-p-tyrosine en
dc.subject dopamine en
dc.subject paradoxical sleep deprivation en
dc.subject Parkinson's disease en
dc.subject reserpine en
dc.subject rotenone en
dc.title Paradoxical Sleep Deprivation Modulates Tyrosine Hydroxylase Expression in the Nigrostriatal Pathway and Attenuates Motor Deficits Induced by Dopaminergic Depletion en
dc.type Artigo
dc.contributor.institution Univ Fed Parana
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ Fed Parana, Dept Fisiol, Setor Ciencias Biol, BR-81531990 Curitiba, Parana, Brazil
dc.description.affiliation Univ Fed Sao Paulo, Dept Psicobiol, Sao Paulo, Brazil
dc.description.affiliation Univ Fed Parana, Dept Farmacol, BR-81531990 Curitiba, Parana, Brazil
dc.description.affiliationUnifesp Univ Fed Sao Paulo, Dept Psicobiol, Sao Paulo, Brazil
dc.description.sponsorshipID FAPESP: 06/55968-6
dc.description.sponsorshipID FAPESP: 98/14.303-3
dc.identifier.doi 10.2174/187152712800792839
dc.description.source Web of Science
dc.identifier.wos WOS:000304818900005



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