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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.)

Pilocarpine-induced status epilepticus reduces chemosensory control of breathing

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Author(s):
Maia, Octavio A. C. [1] ; Malheiros-Lima, Milene R. [1] ; Oliveira, Maria A. [2] ; Castro, Claudio L. [1] ; Moriya, Henrique T. [3] ; Tavares-de-Lima, Wothan [2] ; Takakura, Ana C. [2] ; Moreira, Thiago S. [1]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, 1524 Prof Lineu Prestes Av, BR-05508000 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Sao Paulo, SP - Brazil
[3] Univ Sao Paulo, Dept Engn Control & Telecommun, Sao Paulo, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Brain Research Bulletin; v. 161, p. 98-105, AUG 2020.
Web of Science Citations: 1
Abstract

One of the possible causes of death in epilepsy is breathing disorders, especially apneas, which lead to an increase in CO2 levels (hypercapnia) and/or a decrease in O-2 levels in arterial blood (hypoxemia). The respiratory neurons located in the ventral brainstem respiratory column are the main groups responsible for controlling breathing. Recent data from our group demonstrated respiratory changes in two experimental models of epilepsy, i.e. audiogenic epilepsy, and amygdala rapid kindling. Here, we aimed to evaluate respiratory changes in the classic model of temporal lobe epilepsy induced by intra-hippocampal injection of pilocarpine. Adult Wistar rats with stainless-steel cannulas implanted in the hippocampus region were used. The animals were submitted to pilocarpine injection (2.4 mg/mu L, N = 12-15) or saline (N = 9) into the hippocampus. The respiratory parameters analyzed by whole-body plethysmography were respiratory rate (f(R)), tidal volume (V-T) and ventilation (V-E). Respiratory mechanics such as Newtonian airway resistance (R-n), viscance of the pulmonary parenchyma (G) and the elastance of the pulmonary parenchyma (H) were also investigated. No changes in baseline breathing were detected 15 or 30 days after pilocarpine-induced status epilepticus (SE). However, 30 days after pilocarpine-induced SE, a significant reduction in V-E was observed during hypercapnic (7% CO2) stimulation, without affecting the hypoxia (8% O-2) ventilatory response. We also did not observe changes in respiratory mechanics. The present results suggest that the impairment of the hypercapnia ventilatory response in pilocarpine-induced SE could be related to a presumable degeneration of brainstem respiratory neurons but not to peripheral mechanisms. (AU)

FAPESP's process: 15/23376-1 - Retrotrapezoid nucleus, respiratory chemosensitivity and breathing automaticity
Grantee:Thiago dos Santos Moreira
Support Opportunities: Research Projects - Thematic Grants
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: 17/08696-5 - Purinergic signalling within the Retrotrapezoid Nucleus region: role of breathing control in the temporal lobe epilepsy model
Grantee:Milene Rodrigues Malheiros Lima
Support Opportunities: Scholarships in Brazil - Post-Doctoral