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Acta Physiologica 2008; Volume 192, Supplement 661
Belgian Society for Fundamental and Clinical Physiology and Pharmacology, Spring Meeting 2007
4/21/2007-4/24/2007
University of Antwerp, Antwerp, Belgium
VAGUS NERVE COMPOUND ACTION POTENTIALS (CAPS) VERIFY VAGUS NERVE STIMULATION (VNS) IN RATS
Abstract number: PO-10
Waterschoot1 L., Raedt1 R., De Smedt1 T., Wyckhuys1 T., De Herdt1 V., Van Dycke1 A., Delbeke J., Vonck1 K., Wadman W., Boon1 P.
1Reference Centre for Refractory Epilepsy and Laboratory for Clinical and Experimental Neurophysiology, Department of Neurology, Ghent University Hospital, Ghent, Belgium
Neural Rehabilitation Engineering Laboratory, Department of Physiology and Pharmacology, Universit Catholique de Louvain, Brussels, Belgium
Centre for Neuroscience, University of Amsterdam, Amsterdam, the Netherlands.
Purpose: Vagus nerve stimulation (VNS) is an adjunctive therapy for patients with refractory epilepsy. Although the efficacy and safety of VNS has been demonstrated, the mechanism of action remains to be elucidated. The anti-epileptic effect of VNS may be dependent on the type of nerve fibre being stimulated. Therefore, to know which fibres are activated when stimulating the vagus nerve in rats, simultaneous stimulating and recording is performed to obtain stimulus/response curves. Method: A custom made self-sizing spiral silicone cuff-electrode was implanted around the vagus nerve and a monopolar recording electrode was placed on the nerve. Electrophysiological measurements of compound action potentials (CAP) of the vagus nerve were performed under deep xylazine/ketamine anesthesia. Several combinations of stimulation parameters (amplitude: 0-2.5mA, pulse width: 0.08ms, frequency: 1Hz, pulse duration: 1s) were tested in different configurations (recording electrode placed rostrally/caudally to the stimulation electrode and negative pole of the stimulating electrode placed rostrally/caudally) using a referential montage. Results: In all configurations, stimulation of the vagus nerve elicited compound action potentials with an obvious fast and slow component and stimulus/response curves could be generated. The fast component probably represents A-fibres, while B-fibres might correspond to the slower component. Conclusion: Vagus nerve stimulation intensities used in animal research (0.75mA) would activate the myelinated A- and B-fibres. Further data is needed to measure C-fibre activity. The obtained compound action potentials of these fibres do not imply anti-epileptic properties of VNS, but confirm true vagus nerve stimulation.
To cite this abstract, please use the following information:
Acta Physiologica 2008; Volume 192, Supplement 661 :PO-10