Myo-Inositol Treatment and Gaba-a Receptor Subunit Changes After Kainate- Induced Status Epilepticus

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  • Topic: Hippocampus, Epilepsy, GABAA receptor
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Cellular and Molecular Neurobiology
ISSN 0272-4340
Volume 33
Number 1
Cell Mol Neurobiol (2013) 33:119-127
DOI 10.1007/s10571-012-9877-4
Myo-Inositol Treatment and GABA-A
Receptor Subunit Changes After Kainate-
Induced Status Epilepticus
Revaz Solomonia, Nana Gogichaishvili,
Maia Nozadze, Eka Lepsveridze, David
Dzneladze & Tamar Kiguradze
123
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ORIGINAL RESEARCH
Myo-Inositol Treatment and GABA-A Receptor Subunit Changes
After Kainate-Induced Status Epilepticus
Revaz Solomonia • Nana Gogichaishvili •
Maia Nozadze • Eka Lepsveridze • David Dzneladze •
Tamar Kiguradze
Received: 16 July 2012 / Accepted: 17 August 2012 / Published online: 18 September 2012  Springer Science+Business Media, LLC 2012
Abstract Identification of compounds preventing the
biochemical changes that underlie the epileptogenesis
process is of great importance. We have previously shown
that myo-Inositol (MI) daily treatment prevents certain
biochemical changes that are triggered by kainic acid
(KA)-induced status epilepticus (SE). The aim of the current work was to study the further influence of MI treatment
on the biochemical changes of epileptogenesis and
focus on changes in the hippocampus and neocortex of rats
for the following GABA-A receptor subunits: a1, a4, c2,
and d. After SE, one group of rats was treated with saline,
while the second group was treated with MI. Control
groups that were not treated by the convulsant received
either saline or MI administration. 28–30 h after the
experiment, a decrease in the amount of the a1 subunit was
revealed in the hippocampus and MI had no significant
influence on it. On the 28th day of the experiment, the
amount of a1 was increased in both the KA- and
KA ? MI-treated groups. The a4 and c2 subunits were
strongly reduced in the hippocampus of KA-treated animals,
but MI significantly halted this reduction. The effects
of MI on a4 and c2 subunit changes were significantly
different between hippocampus and neocortex. On the
twenty-eighth day after SE, a decrease in the amount of a1
was found in the neocortex, but MI treatment had no effect
on it. The obtained results indicate that MI treatment
interferes with some of the biochemical processes of
epileptogenesis.
Keywords Epilepsy  Kainic acid  Epileptogenesis 
Myo-Inositol  c-Aminobutyric acid receptor subunits
Introduction
Epilepsy is a heterogeneous group of disorders. It is the
most common neurologic disorder after stroke, with a
2–3 % life time risk that a patient may receive a diagnosis of epilepsy (Browne and Holmes 2001). The available
therapy against epilepsy is only symptomatic and often
ineffective (Loescher et al. 2008). The most important
challenge is to prevent the process of epileptogenesis
(Loescher et al. 2008), not merely to treat its symptoms. At present, there is no anti-epileptic drug (AED) that performs this function (Loescher et al. 2008). Thus, the search for
truly anti-epileptogenic drugs is of outstanding importance
for modern biomedical sciences.
A series of our previous experiments have revealed that a
water extract of the medicinal plant Aquilegia vulgaris contains compounds that alter the binding of ligands to the benzodiazepine and c-aminobutyric acid (GABA) binding sites of
the GABA-A receptors (GABA-AR) (Solomonia et al. 2004).
We have identified two main active compounds from this
extract: (1) myo-Inositol (MI) and (2)...
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