Inflammatory Sensitization of Vagal TRPV1 Receptors Leads to Respiratory Alkalosis and Increased Susceptibility to Febrile Seizures
Abstract number :
1.062
Submission category :
1. Basic Mechanisms / 1E. Models
Year :
2021
Submission ID :
1826667
Source :
www.aesnet.org
Presentation date :
12/4/2021 12:00:00 PM
Published date :
Nov 22, 2021, 06:55 AM
Authors :
Karlene Barrett, PhD - Cumming School of Medicine, University of Calgary; Arijit Roy, PhD - Research Associate, Pediatrics, Cumming School of Medicine, University of Calgary; Richard Wilson, PhD - Professor, Cumming School of Medicine, University of Calgary; Quentin Pittman, PhD - Professor, Cumming School of Medicine, University of Calgary; Morris Scantlebury, MD - Associate Professor, Cumming School of Medicine, University of Calgary
Rationale: Febrile seizures (FS) account for ~20% of all pediatric neurological disorders and are the most common convulsive seizure disorder to affect infants and children. Whether simple or complex, FS are not always benign. Simple FS increase the risk of cognitive deficits in babies < 1-year-old and the risk of sudden unexpected death in childhood. Complex FS increase the risk of developing epilepsy 8-fold. The mechanism underlying FS is likely multifactorial and probably involves a complex interaction between inflammation, fever, and alterations in the acid-base balance. Increasing evidence suggests a link between fever-induced respiratory alkalosis and an increased risk of FS in both human and experimental animals, however, the neuro-anatomical and molecular mechanisms involved are poorly understood. In this study we hypothesize that inflammatory sensitization and heat activation of vagal TRPV1 receptors contribute to FS genesis.
Basic Mechanisms