This article is part of the Research Topic Brain oscillations and behavior.

Original Research ARTICLE

Front. Integr. Neurosci., 15 June 2009 | doi: 10.3389/neuro.07.013.2009

Cannabinoid receptor activation reverses kainate-induced synchronized population burst firing in rat hippocampus

1
School of Biomedical Sciences, University of Nottingham Medical School, Queen’s Medical Centre, Nottingham, UK
2
Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD, USA
Cannabinoids have been shown to possess anticonvulsant properties in whole animal models of epilepsy. The present investigation sought to examine the effects of cannabinoid receptor activation on kainic acid (KA)-induced epileptiform neuronal excitability. Under urethane anesthesia, acute KA treatment (10 mg kg−1, i.p.) entrained the spiking mode of simultaneously recorded neurons from random firing to synchronous bursting (% change in burst rate). Injection of the high-affinity cannabinoid agonist (-)-11-hydroxy-8-tetrahydrocannabinol-dimethyl-heptyl (HU210, 100 μg kg−1, i.p.) following KA markedly reduced the burst frequency (% decrease in burst frequency) and reversed synchronized firing patterns back to baseline levels. Pre-treatment with the central cannabinoid receptor (CB1) antagonist N-piperidino-5-(4-clorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide (rimonabant, SR141716A 3 mg kg−1, i.p.) completely prevented the actions of HU210. The present results indicate that cannabinoids exert their antiepileptic effects by impeding pathological synchronization of neuronal networks in the hippocampus.
Keywords:
CB1 receptor, multiple single-neuron recording, urethane, GABA
Citation:
Mason R and Cheer JF (2009). Cannabinoid receptor activation reverses kainate-induced synchronized population burst firing in rat hippocampus. Front. Integr. Neurosci. 3:13. doi:10.3389/neuro.07.013.2009
Received:
20 February 2009;
 Paper pending published:
12 May 2009;
Accepted:
02 June 2009;
 Published online:
15 June 2009.

Edited by:

Rui M. Costa, Instituto Gulbenkian de Ciência, Portugal

Reviewed by:

David M. Lovinger, National Institute on Alcohol Abuse and Alcoholism, NIH, USA
Henry H. Yin, Duke University, USA
Copyright:
© 2009 Mason and Cheer. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
*Correspondence:
Joseph F. Cheer, Department of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn Street, HSF I, Baltimore, MD 21201, USA. e-mail: jchee001@umaryland.edu
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