Neuroscience 2005 Abstract
| Presentation Number: | 782.10 |
|---|---|
| Abstract Title: | The effects of cannabidiol in a kainate model of temporal lobe epilepsy. |
| Authors: |
Coomber, B.*1
; Spicer, C. H.1
; O'Donoghue, M.2
; Mason, R.1
1School of Biomedical Sciences, Univ. of Nottingham Med. School, Nottingham, United Kingdom 2Department of Neurology QMC, Univ. of Nottingham Med. School, Nottingham, United Kingdom |
| Primary Theme and Topics |
Disorders of the Nervous System - Epilepsy -- Basic mechanisms |
| Session: |
782. Epilepsy: Basic Mechanisms III Poster |
| Presentation Time: | Tuesday, November 15, 2005 2:00 PM-3:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # SS30 |
| Keywords: | CANNABINOIDS, SEIZURE, MULTIELECTRODE, HIPPOCAMPUS |
Cannabinoids, including cannabidiol (CBD), a non-psychoactive component of cannabis sativa, have been shown to exhibit anticonvulsant properties in animal models of epilepsy (Wallace et al. 2001; 2003). To investigate cannabinoid-mediated seizure control, CBD was compared to the synthetic CB1 receptor agonist HU-210 in a rat model of kainate-induced temporal lobe seizures (TLS) in vivo.
Multiple single-unit and local field potentials (LFPs) were recorded from the hippocampus of male Sprague Dawley rats (200-300g) anaesthetised with urethane (1.3g kg-1 i.p.) or isoflurane/N2O/O2 using 16-channel micro-wire electrodes (NB Labs) and a Plexon Map system. Kainate (KA: 10mg kg-1), cannabidiol (10 or 40mg kg-1) or HU-210 (100μg kg-1) were administered i.p. Data was analysed with Neuroexplorer, including firing frequency, burst analysis, T50 for KA-induced effects, and LFP power spectral density (PSD).
While CBD reduced basal firing in ∼20% of cells, CBD did not alter KA-induced firing administered before (n=63 cells) or after (n=24 cells) KA. CBD (10mg kg-1) extended the T50 for KA-induced firing onset up to 15mins. In contrast, HU-210 reduced KA-evoked firing (n=19 cells, p<0.05).
KA increased the power in all frequency bands of the LFP PSD, particularly a peak shift from 1 to 5Hz with additional bands around 30Hz and 50Hz compared to basal. This was unaffected by CBD before or after KA injection. CBD caused a shift in power in the γ-band (24-40Hz) in CA3 corresponding to a small reduction in unit firing frequency. HU-210 reduced PSD in all LFP frequency bands when administered after KA.
We conclude that CBD is a less potent anticonvulsant than HU-210, and suggest that CB1 receptors may be central to cannabinoid-mediated anticonvulsant activity.
Multiple single-unit and local field potentials (LFPs) were recorded from the hippocampus of male Sprague Dawley rats (200-300g) anaesthetised with urethane (1.3g kg-1 i.p.) or isoflurane/N2O/O2 using 16-channel micro-wire electrodes (NB Labs) and a Plexon Map system. Kainate (KA: 10mg kg-1), cannabidiol (10 or 40mg kg-1) or HU-210 (100μg kg-1) were administered i.p. Data was analysed with Neuroexplorer, including firing frequency, burst analysis, T50 for KA-induced effects, and LFP power spectral density (PSD).
While CBD reduced basal firing in ∼20% of cells, CBD did not alter KA-induced firing administered before (n=63 cells) or after (n=24 cells) KA. CBD (10mg kg-1) extended the T50 for KA-induced firing onset up to 15mins. In contrast, HU-210 reduced KA-evoked firing (n=19 cells, p<0.05).
KA increased the power in all frequency bands of the LFP PSD, particularly a peak shift from 1 to 5Hz with additional bands around 30Hz and 50Hz compared to basal. This was unaffected by CBD before or after KA injection. CBD caused a shift in power in the γ-band (24-40Hz) in CA3 corresponding to a small reduction in unit firing frequency. HU-210 reduced PSD in all LFP frequency bands when administered after KA.
We conclude that CBD is a less potent anticonvulsant than HU-210, and suggest that CB1 receptors may be central to cannabinoid-mediated anticonvulsant activity.
Supported by The MRC and University of Nottingham
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
Copyright © 2005-2025 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.
