Myo‐Inositol Limits Kainic Acid‐Induced Epileptogenesis in Rats
(2022) In International Journal of Molecular Sciences 23(3).- Abstract
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. Cur-rently, 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... (More)
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. Cur-rently, 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 elec-trographic 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 coun-teract 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.
(Less)
- author
- Kandashvili, Manana ; Gamkrelidze, Georgi ; Tsverava, Lia ; Lordkipanidze, Tamar ; Lepsveridze, Eka ; Lagani, Vincenzo ; Burjanadze, Maia ; Dashniani, Manana ; Kokaia, Merab LU and Solomonia, Revaz
- publishing date
- 2022
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Electrographic seizures, Epilepsy, Epileptogenesis, Glial fibrillary acidic protein, Kainic acid, Learning and memory, Myo‐inositol, Protein tyrosine phosphatase receptor type R, Volume regulated anionic channel
- in
- International Journal of Molecular Sciences
- volume
- 23
- issue
- 3
- article number
- 1198
- publisher
- MDPI AG
- external identifiers
-
- scopus:85122995987
- pmid:35163126
- ISSN
- 1661-6596
- DOI
- 10.3390/ijms23031198
- language
- English
- LU publication?
- no
- id
- 6eb11870-1d97-4ae1-b300-50b9d54521ab
- date added to LUP
- 2022-03-02 11:25:46
- date last changed
- 2024-06-27 12:38:32
@article{6eb11870-1d97-4ae1-b300-50b9d54521ab,
abstract = {{<p>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. Cur-rently, 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 elec-trographic 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 coun-teract 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.</p>}},
author = {{Kandashvili, Manana and Gamkrelidze, Georgi and Tsverava, Lia and Lordkipanidze, Tamar and Lepsveridze, Eka and Lagani, Vincenzo and Burjanadze, Maia and Dashniani, Manana and Kokaia, Merab and Solomonia, Revaz}},
issn = {{1661-6596}},
keywords = {{Electrographic seizures; Epilepsy; Epileptogenesis; Glial fibrillary acidic protein; Kainic acid; Learning and memory; Myo‐inositol; Protein tyrosine phosphatase receptor type R; Volume regulated anionic channel}},
language = {{eng}},
number = {{3}},
publisher = {{MDPI AG}},
series = {{International Journal of Molecular Sciences}},
title = {{Myo‐Inositol Limits Kainic Acid‐Induced Epileptogenesis in Rats}},
url = {{http://dx.doi.org/10.3390/ijms23031198}},
doi = {{10.3390/ijms23031198}},
volume = {{23}},
year = {{2022}},
}