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Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats
Epilepsy is a severe neurological disease characterized by spontaneous recurrent seizures (SRS). A complex pathophysiological process referred to as epileptogenesis transforms a normal brain into an epileptic one. Prevention of epileptogenesis is a subject of intensive research. Currently, there are...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835653/ https://www.ncbi.nlm.nih.gov/pubmed/35163126 http://dx.doi.org/10.3390/ijms23031198 |
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author | Kandashvili, Manana Gamkrelidze, Georgi Tsverava, Lia Lordkipanidze, Tamar Lepsveridze, Eka Lagani, Vincenzo Burjanadze, Maia Dashniani, Manana Kokaia, Merab Solomonia, Revaz |
author_facet | Kandashvili, Manana Gamkrelidze, Georgi Tsverava, Lia Lordkipanidze, Tamar Lepsveridze, Eka Lagani, Vincenzo Burjanadze, Maia Dashniani, Manana Kokaia, Merab Solomonia, Revaz |
author_sort | Kandashvili, Manana |
collection | PubMed |
description | Epilepsy is a severe neurological disease characterized by spontaneous recurrent seizures (SRS). A complex pathophysiological process referred to as epileptogenesis transforms a normal brain into an epileptic one. Prevention of epileptogenesis is a subject of intensive research. Currently, there are no clinically approved drugs that can act as preventive medication. Our previous studies have revealed highly promising antiepileptogenic properties of a compound–myo-inositol (MI) and the present research broadens previous results and demonstrates the long-term disease-modifying effect of this drug, as well as the amelioration of cognitive comorbidities. For the first time, we show that long-term treatment with MI: (i) decreases the frequency and duration of electrographic SRS in the hippocampus; (ii) has an ameliorating effect on spatial learning and memory deficit associated with epileptogenesis, and (iii) attenuates cell loss in the hippocampus. MI treatment also alters the expression of the glial fibrillary acidic protein, LRRC8A subunit of volume-regulated anion channels, and protein tyrosine phosphatase receptor type R, all expected to counteract the epileptogenesis. All these effects are still present even 4 weeks after MI treatment ceased. This suggests that MI may exert multiple actions on various epileptogenesis-associated changes in the brain and, therefore, could be considered as a candidate target for prevention of epileptogenesis. |
format | Online Article Text |
id | pubmed-8835653 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-88356532022-02-12 Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats Kandashvili, Manana Gamkrelidze, Georgi Tsverava, Lia Lordkipanidze, Tamar Lepsveridze, Eka Lagani, Vincenzo Burjanadze, Maia Dashniani, Manana Kokaia, Merab Solomonia, Revaz Int J Mol Sci Article Epilepsy is a severe neurological disease characterized by spontaneous recurrent seizures (SRS). A complex pathophysiological process referred to as epileptogenesis transforms a normal brain into an epileptic one. Prevention of epileptogenesis is a subject of intensive research. Currently, there are no clinically approved drugs that can act as preventive medication. Our previous studies have revealed highly promising antiepileptogenic properties of a compound–myo-inositol (MI) and the present research broadens previous results and demonstrates the long-term disease-modifying effect of this drug, as well as the amelioration of cognitive comorbidities. For the first time, we show that long-term treatment with MI: (i) decreases the frequency and duration of electrographic SRS in the hippocampus; (ii) has an ameliorating effect on spatial learning and memory deficit associated with epileptogenesis, and (iii) attenuates cell loss in the hippocampus. MI treatment also alters the expression of the glial fibrillary acidic protein, LRRC8A subunit of volume-regulated anion channels, and protein tyrosine phosphatase receptor type R, all expected to counteract the epileptogenesis. All these effects are still present even 4 weeks after MI treatment ceased. This suggests that MI may exert multiple actions on various epileptogenesis-associated changes in the brain and, therefore, could be considered as a candidate target for prevention of epileptogenesis. MDPI 2022-01-21 /pmc/articles/PMC8835653/ /pubmed/35163126 http://dx.doi.org/10.3390/ijms23031198 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Kandashvili, Manana Gamkrelidze, Georgi Tsverava, Lia Lordkipanidze, Tamar Lepsveridze, Eka Lagani, Vincenzo Burjanadze, Maia Dashniani, Manana Kokaia, Merab Solomonia, Revaz Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats |
title | Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats |
title_full | Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats |
title_fullStr | Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats |
title_full_unstemmed | Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats |
title_short | Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats |
title_sort | myo-inositol limits kainic acid-induced epileptogenesis in rats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835653/ https://www.ncbi.nlm.nih.gov/pubmed/35163126 http://dx.doi.org/10.3390/ijms23031198 |
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