Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

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 LU and Solomonia, Revaz (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)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; ; and
publishing date
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
2024-06-13 11:12:14
@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}},
}