| Texto completo | |
| Autor(es): |
Nascimento, Andre L. F.
;
Medeiros, Pamela O. S.
;
Pedrao, Luiz F. A. T.
;
Queiroz, Vitoria C.
;
Oliveira, Luiz M.
;
Novaes, Leonardo S.
;
Caetano, Ariadiny L.
;
Munhoz, Carolina D.
;
Takakura, Ana C.
;
Falquetto, Barbara
Número total de Autores: 10
|
| Tipo de documento: | Artigo Científico |
| Fonte: | Neuroscience; v. 502, p. 16-pg., 2022-10-15. |
| Resumo | |
Parkinson's Disease (PD) is a neurogenerative disorder characterized by the death of dopaminergic neurons in the Substantia Nigra pars compacta (SNpc), leading to motor, cognitive, learning, and respiratory dysfunctions. New evidence revealed that breathing impairment in PD mainly results from oxidative stress (OS) that initiates apoptotic signaling in respiratory neurons. Here, we investigated the role of OS inhibition using apocynin (non-specific NADPH oxidase inhibitor) in a 6-OHDA PD animal model in the neural control of breathing. The PD model was confirmed with a 70% reduction in TH-expressing neurons within the SNpc. After 20 and 40 days of PD induction, no differences were observed in superoxide anion levels in any respiratory nuclei. At 30 days after PD induction, 6-OHDA animals presented OS that was prevented in all respiratory nuclei by adding apocynin to the drinking water for 10 days. Forty days after PD animal model induction, impaired motor and breathing function, reduced Phox2b and NK1 receptors-expressing neurons in the medullary respiratory areas; decreased latency to fall in the rotarod motor test; and attenuated respiratory frequency and minute ventilation parameters at rest and under hypercapnia conditions were observed. After 20 days of apocynin treatment, neurodegeneration of respiratory nuclei and breathing dysfunction in 6-OHDA animals were prevented. Thus, OS contributes to respiratory neuron death, consequently leading to breathing dysfunction in the 6-OHDA PD animal model. Furthermore, these results present a new perspective for preventing the onset and progression of PD-related respiratory impairments. (C) 2022 IBRO. Published by Elsevier Ltd. All rights reserved. (AU) | |
| Processo FAPESP: | 15/23376-1 - Núcleo retrotrapezóide, quimiossensibilidade central e automaticidade respiratória |
| Beneficiário: | Thiago dos Santos Moreira |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 19/00065-1 - Participação do estresse oxidativo na degeneração dos neurônios respiratórios do bulbo no modelo animal de Doença de Parkinson |
| Beneficiário: | Bárbara Falquetto |
| Modalidade de apoio: | Auxílio à Pesquisa - Jovens Pesquisadores |
| Processo FAPESP: | 16/03572-3 - A relação entre a ativação dos receptores de glicocorticoides e a hiperexcitabilidade dos neurônios do complexo basolateral da amígdala na ansiedade tardia induzida por estresse agudo em ratos e sua implicação no déficit de extinção da memória de medo |
| Beneficiário: | Carolina Demarchi Munhoz |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 19/01236-4 - Efeitos de tratamentos farmacológicos e não farmacológicos nas alterações respiratórias observadas em um modelo murino da Doença de Parkinson |
| Beneficiário: | Ana Carolina Takakura Moreira |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |