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Targeting the endocannabinoid system in the amygdala kindling model of temporal lobe epilepsy in mice.
Epilepsia 2011; 52(7):e62-5E

Abstract

The endocannabinoid system can be considered as a putative target to affect ictogenesis as well as the generation of a hyperexcitable epileptic network. Therefore, we evaluated the effect of a CB1 receptor agonist (WIN55.212-2) and of an inhibitor of the enzymatic degradation of the endocannabinoid anandamide (fatty acid hydrolase inhibitor URB597) in the amygdala kindling model of temporal lobe epilepsy. Only minor effects on seizure thresholds and seizure parameters without a clear dose-dependency were observed in fully kindled mice. When evaluating the impact on kindling acquisition, WIN55.212-2 significantly delayed the progression of seizure severity. In contrast, URB597 did not affect the development of seizures in the kindling paradigm. Analysis of cell proliferation and neurogenesis during the kindling process revealed that URB597 significantly reduced the number of newborn neurons. These data give first evidence that CB1-receptor activation might render a disease-modifying approach. Future studies are necessary that further analyze the role of CB1 receptors and to confirm the efficacy of CB1-receptor agonists in other models of chronic epilepsy.

Authors+Show Affiliations

Institute of Pharmacology, Toxicology, and Pharmacy, Ludwig-Maximilians-University, Koeniginstrasse 16, Munich, Germany.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21627644

Citation

Wendt, Hannes, et al. "Targeting the Endocannabinoid System in the Amygdala Kindling Model of Temporal Lobe Epilepsy in Mice." Epilepsia, vol. 52, no. 7, 2011, pp. e62-5.
Wendt H, Soerensen J, Wotjak CT, et al. Targeting the endocannabinoid system in the amygdala kindling model of temporal lobe epilepsy in mice. Epilepsia. 2011;52(7):e62-5.
Wendt, H., Soerensen, J., Wotjak, C. T., & Potschka, H. (2011). Targeting the endocannabinoid system in the amygdala kindling model of temporal lobe epilepsy in mice. Epilepsia, 52(7), pp. e62-5. doi:10.1111/j.1528-1167.2011.03079.x.
Wendt H, et al. Targeting the Endocannabinoid System in the Amygdala Kindling Model of Temporal Lobe Epilepsy in Mice. Epilepsia. 2011;52(7):e62-5. PubMed PMID: 21627644.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeting the endocannabinoid system in the amygdala kindling model of temporal lobe epilepsy in mice. AU - Wendt,Hannes, AU - Soerensen,Jonna, AU - Wotjak,Carsten T, AU - Potschka,Heidrun, Y1 - 2011/05/31/ PY - 2011/6/2/entrez PY - 2011/6/2/pubmed PY - 2011/9/14/medline SP - e62 EP - 5 JF - Epilepsia JO - Epilepsia VL - 52 IS - 7 N2 - The endocannabinoid system can be considered as a putative target to affect ictogenesis as well as the generation of a hyperexcitable epileptic network. Therefore, we evaluated the effect of a CB1 receptor agonist (WIN55.212-2) and of an inhibitor of the enzymatic degradation of the endocannabinoid anandamide (fatty acid hydrolase inhibitor URB597) in the amygdala kindling model of temporal lobe epilepsy. Only minor effects on seizure thresholds and seizure parameters without a clear dose-dependency were observed in fully kindled mice. When evaluating the impact on kindling acquisition, WIN55.212-2 significantly delayed the progression of seizure severity. In contrast, URB597 did not affect the development of seizures in the kindling paradigm. Analysis of cell proliferation and neurogenesis during the kindling process revealed that URB597 significantly reduced the number of newborn neurons. These data give first evidence that CB1-receptor activation might render a disease-modifying approach. Future studies are necessary that further analyze the role of CB1 receptors and to confirm the efficacy of CB1-receptor agonists in other models of chronic epilepsy. SN - 1528-1167 UR - https://www.unboundmedicine.com/medline/citation/21627644/Targeting_the_endocannabinoid_system_in_the_amygdala_kindling_model_of_temporal_lobe_epilepsy_in_mice_ L2 - https://doi.org/10.1111/j.1528-1167.2011.03079.x DB - PRIME DP - Unbound Medicine ER -