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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Amygdala rapid kindling impairs breathing in response to chemoreflex activation

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Author(s):
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]
Total Authors: 8
Affiliation:
[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
Total Affiliations: 4
Document type: Journal article
Source: Brain Research; v. 1718, p. 159-168, SEP 1 2019.
Web of Science Citations: 1
Abstract

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)

FAPESP's process: 16/23281-3 - Encephalic regions responsible for neuroplasticity observed in respiratory response induced by hypercapnia in a modelo of Parkinson's Disease
Grantee:Ana Carolina Takakura Moreira
Support Opportunities: Regular Research Grants
FAPESP's process: 05/56447-7 - Research through images from high field magnetic resonance aimed at studies in humans
Grantee:João Pereira Leite
Support Opportunities: Inter-institutional Cooperation in Support of Brain Research (CINAPCE) - Thematic Grants
FAPESP's process: 15/23376-1 - Retrotrapezoid nucleus, respiratory chemosensitivity and breathing automaticity
Grantee:Thiago dos Santos Moreira
Support Opportunities: Research Projects - Thematic Grants