Cardiorespiratory response to hypercapnia across epileptogenesis in the kainic acid model
Abstract number :
3.241
Submission category :
3. Neurophysiology / 3F. Animal Studies
Year :
2025
Submission ID :
139
Source :
www.aesnet.org
Presentation date :
12/8/2025 12:00:00 AM
Published date :
Authors :
Presenting Author: Auriane Apaire, PhD – Université Catholique de Louvain, Institute of Neuroscience (IoNS), Clinical Neuroscience, Brussels, Belgium
Abigaïl Niyibizi, Student – Université Catholique de Louvain, Institute of Neuroscience (IoNS), Clinical Neuroscience, Brussels, Belgium
Ayse Dereli, postdoc – Université Catholique de Louvain, Institute of Neuroscience (IoNS), Clinical Neuroscience, Brussels, Belgium
Riëm El Tahry, MD, PhD – Université Catholique de Louvain, Clinique Universitaire ST Luc
Rationale: Central apnea accompanied by cardiac abnormalities appears to be a key contributor to sudden unexpected death in epilepsy (SUDEP). In particular, dysregulation of central CO₂ chemoreception (CCR)—the system that detects changes in PCO₂ levels—is thought to play a role in SUDEP, along with autonomic disturbance. CCR can be assessed through the ventilatory response to a hypercapnic challenge; however, it has not been previously examined during epileptogenesis in a chronic model of temporal lobe epilepsy, where SUDEP may occur.
Methods: We aimed to investigate cardiorespiratory responses to acute hypercapnia throughout epileptogenesis in the kainic acid (KA) model. Sprague-Dawley rats received intrahippocampal KA injections to induce severe spontaneous seizures, typically emerging after four months. Cardiorespiratory responses were recorded before the injection and then monthly for six months post-injection. Using photoplethysmography, we measured interictal ventilatory frequency (fB), heart rate (HR), and oxygen saturation (PO₂) before, during, and after a 1-hour exposure to 10% CO₂. Electroencephalography was used to monitor epileptogenesis and assess the severity of epilepsy.
Results: Results showed that oxygen saturation (PO₂) remained stable at approximately 100% throughout the study. However, the ventilatory frequency (fB) response to 10% CO₂ was significantly reduced in correlation with epilepsy severity at months four, five, and six compared to baseline (p < 0.0001, p < 0.0001, and p < 0.001, respectively; 2-way ANOVA, Fisher’s LSD test). In contrast, the heart rate (HR) response to 10% CO₂ was significantly elevated at months one, three, and four (p < 0.05, p < 0.0001, and p < 0.0001, respectively) but was abolished by months five and six.
Neurophysiology