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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Amygdala rapid kindling impairs breathing in response to chemoreflex activation

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Autor(es):
Totola, Leonardo T. [1] ; Malheiros-Lima, Milene R. [1] ; Delfino-Pereira, Polianna [2] ; Del Vecchio, Flavio [3] ; Souza, Felipe C. [4] ; Takakura, Ana C. [4] ; Garcia-Cairasco, Norberto [2, 3] ; Moreira, Thiago S. [1]
Número total de Autores: 8
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, 1524 Prof Lineu Prestes Ave, BR-05508000 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Neurosci & Behav Sci, BR-14049900 Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Physiol, 3900 Bandeirantes Ave, BR-14049900 Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508000 Sao Paulo, SP - Brazil
Número total de Afiliações: 4
Tipo de documento: Artigo Científico
Fonte: Brain Research; v. 1718, p. 159-168, SEP 1 2019.
Citações Web of Science: 1
Resumo

Temporal lobe epilepsy is often accompanied by behavioral, electroencephalographic and autonomic abnormalities. Amygdala kindling has been used as an experimental model to study epileptogenesis. Although amygdala kindling has been extensively investigated in the context of its clinical relevance to the epilepsies, potential associated respiratory alterations are not well known. Here, our main objective was to better investigate the mechanisms involved in respiratory physiology impairment in the amygdala rapid kindling (ARK) model of epileptogenesis. Male Wistar rats with electrodes implanted into the amygdaloid complex were used. After recovery from surgery, the rats were subjected to electrical stimulation of basolateral amygdala for 2 consecutive days (10 stimuli/day). The ventilatory parameters were evaluated by whole body plethysmography. Thereafter, animals were also exposed to hypercapnia (7% CO2) for 3 h to evaluate fos protein expression in several nuclei involved in respiratory control. We observed a significant reduction in ventilation during the ictal phase elicited by ARK. We also found that 10 days after ARK, baseline ventilation as well as the hypercapnia ventilatory response (7% CO2) were reduced compared to control rats. The number of fos-immunoreactive neurons in the retrotrapezoid nucleus, raphe magnus and nucleus of the solitary tract were also reduced after ARK. Our results showed that ARK was able to impair breathing function, demonstrating a strong coupling between amygdala and the respiratory neurons in the brainstem, with potential impact in respiratory failures, frequently fatal, during or after epileptic seizures in chronic animal models and in patients. (AU)

Processo FAPESP: 07/50261-4 - Neurociências, epilepsia e arte: caracterização interdisciplinar da cepa WAR e modelos de epilepsia correlacionados: as oficinas Da Vinci, divulgação científica e quebras de estigmas em epilepsia
Beneficiário:Norberto Garcia Cairasco
Modalidade de apoio: Auxílio à Pesquisa - Temático
Processo FAPESP: 16/23281-3 - Regiões encefálicas responsáveis pela neuroplasticidade observada na resposta respiratória induzida por hipercapnia em modelo animal de Doença de Parkinson
Beneficiário:Ana Carolina Takakura Moreira
Modalidade de apoio: Auxílio à Pesquisa - Regular
Processo FAPESP: 05/56447-7 - Pesquisa através de imagens por ressonância magnética de alto campo destinadas a estudos em humanos
Beneficiário:João Pereira Leite
Modalidade de apoio: Auxílio à Pesquisa - Programa CINAPCE - Temático
Processo FAPESP: 15/23376-1 - Núcleo retrotrapezóide, quimiossensibilidade central e automaticidade respiratória
Beneficiário:Thiago dos Santos Moreira
Modalidade de apoio: Auxílio à Pesquisa - Temático