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Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy

Canine drug-resistant epilepsy is a prevailing issue in veterinary neurology. Alternative or additional treatment with cannabinoids is showing promising results in seizure management. A crucial component of the endocannabinoid system, cannabinoid receptor type 1 (CB1R), is heavily involved in the co...

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Autores principales: Kostic, D., Nowakowska, M., Freundt Revilla, J., Attig, F., Rohn, K., Gualtieri, F., Baumgärtner, W., Potschka, H., Tipold, A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9950490/
https://www.ncbi.nlm.nih.gov/pubmed/36823232
http://dx.doi.org/10.1038/s41598-023-29868-3
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author Kostic, D.
Nowakowska, M.
Freundt Revilla, J.
Attig, F.
Rohn, K.
Gualtieri, F.
Baumgärtner, W.
Potschka, H.
Tipold, A.
author_facet Kostic, D.
Nowakowska, M.
Freundt Revilla, J.
Attig, F.
Rohn, K.
Gualtieri, F.
Baumgärtner, W.
Potschka, H.
Tipold, A.
author_sort Kostic, D.
collection PubMed
description Canine drug-resistant epilepsy is a prevailing issue in veterinary neurology. Alternative or additional treatment with cannabinoids is showing promising results in seizure management. A crucial component of the endocannabinoid system, cannabinoid receptor type 1 (CB1R), is heavily involved in the control of neurotransmitter release. Knowledge of its distribution in the epileptic brain would serve a better understanding of disease pathology and application of cannabinoids in dogs with epilepsy. CB1R distribution was assessed in sub-regions of hippocampus of dogs with idiopathic epilepsy, structural epilepsy and without cerebral pathology. In dogs with idiopathic epilepsy, significantly decreased CB1R expression compared to control animals was observed in CA1. In dogs with structural epilepsy, a significant increase in CB1R signal intensity in comparison to controls was observed. CB1R expression was higher in the structural group as compared to the idiopathic. Double immunofluorescence showed co-localization between CB1R and an astrocytic marker in about 50% of cells, regardless of the diagnosis. In summary, CB1R expression in canine hippocampus undergoes modification by the epileptic process and the direction of this change depends on the etiology of the disease. The distinct disease-associated CB1R expression needs to be considered in new treatment development for dogs with epilepsy.
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spelling pubmed-99504902023-02-25 Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy Kostic, D. Nowakowska, M. Freundt Revilla, J. Attig, F. Rohn, K. Gualtieri, F. Baumgärtner, W. Potschka, H. Tipold, A. Sci Rep Article Canine drug-resistant epilepsy is a prevailing issue in veterinary neurology. Alternative or additional treatment with cannabinoids is showing promising results in seizure management. A crucial component of the endocannabinoid system, cannabinoid receptor type 1 (CB1R), is heavily involved in the control of neurotransmitter release. Knowledge of its distribution in the epileptic brain would serve a better understanding of disease pathology and application of cannabinoids in dogs with epilepsy. CB1R distribution was assessed in sub-regions of hippocampus of dogs with idiopathic epilepsy, structural epilepsy and without cerebral pathology. In dogs with idiopathic epilepsy, significantly decreased CB1R expression compared to control animals was observed in CA1. In dogs with structural epilepsy, a significant increase in CB1R signal intensity in comparison to controls was observed. CB1R expression was higher in the structural group as compared to the idiopathic. Double immunofluorescence showed co-localization between CB1R and an astrocytic marker in about 50% of cells, regardless of the diagnosis. In summary, CB1R expression in canine hippocampus undergoes modification by the epileptic process and the direction of this change depends on the etiology of the disease. The distinct disease-associated CB1R expression needs to be considered in new treatment development for dogs with epilepsy. Nature Publishing Group UK 2023-02-23 /pmc/articles/PMC9950490/ /pubmed/36823232 http://dx.doi.org/10.1038/s41598-023-29868-3 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Kostic, D.
Nowakowska, M.
Freundt Revilla, J.
Attig, F.
Rohn, K.
Gualtieri, F.
Baumgärtner, W.
Potschka, H.
Tipold, A.
Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy
title Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy
title_full Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy
title_fullStr Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy
title_full_unstemmed Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy
title_short Hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy
title_sort hippocampal expression of the cannabinoid receptor type 1 in canine epilepsy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9950490/
https://www.ncbi.nlm.nih.gov/pubmed/36823232
http://dx.doi.org/10.1038/s41598-023-29868-3
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