08.08.2019
 Essay on Myo-Inositol Treatment and Gaba-a Receptor Subunit Changes Following Kainate- Caused Status Epilepticus

123

Cellular and Molecular Neurobiology

ISSN 0272-4340

Volume thirty-three

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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UNIQUE RESEARCH

Myo-Inositol Treatment and GABA-A Radio Subunit Changes

After Kainate-Induced Status Epilepticus

Revaz Solomonia • Ni?era Gogichaishvili •

Maia Nozadze • Eka Lepsveridze • David Dzneladze •

Tamar Kiguradze

Received: 16 Come july 1st 2012 / Accepted: seventeen August 2012 / Posted online: 18 September 2012 Springer Science+Business Media, LLC 2012

Subjective Identification of compounds protecting against 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 which might be triggered by simply kainic acid

(KA)-induced status epilepticus (SE). The aim of the existing work was going to study the further affect of MI treatment

around the biochemical alterations of epileptogenesis and

concentrate on changes in the hippocampus and neocortex of mice

for the following GABA-A radio subunits: a2, a4, c2,

and d. After SONY ERICSSON, one band of rats was treated with saline,

even though the second group was treated with MI. Control

organizations that were certainly not treated by the convulsant received

either saline or MI administration. 28–30 h after the

experiment, a decrease in the number of the a2 subunit was

revealed in the hippocampus and MI acquired no significant

influence into it. On the 29th day from the experiment, the

amount of a1 was increased in both the KA- and

KA? MI-treated organizations. The a4 and c2 subunits had been

strongly decreased in the hippocampus of KA-treated animals,

yet MI drastically halted this reduction. The consequences

of MI on a4 and c2 subunit changes were significantly

different between hippocampus and neocortex. Within the

twenty-eighth day after ZE, a decline in the amount of a1

was present in the neocortex, but MI treatment got no impact

on it. The obtained results indicate that MI treatment

interferes with some of the biochemical operations of

epileptogenesis.

Keywords Epilepsy Kainic acid solution Epileptogenesis

Myo-Inositol c-Aminobutyric acid radio subunits

Introduction

Epilepsy can be described as heterogeneous number of disorders. It is the

most common neurologic disorder following stroke, with a

2–3 % life time risk that a individual may obtain a diagnosis of epilepsy (Browne and Holmes 2001). The obtainable

therapy against epilepsy is only symptomatic and quite often

ineffective (Loescher et al. 2008). The main

challenge is usually to prevent the procedure for epileptogenesis

(Loescher et 's. 2008), not merely to treat their symptoms. Presently, there is no anti-epileptic drug (AED) that functions this function (Loescher ain al. 2008). Thus, the search for

genuinely anti-epileptogenic drugs is of excellent importance

to get modern biomedical sciences.

Several our past experiments have got revealed that a

water get 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 pain (GABA-AR) (Solomonia et approach. 2004).

We certainly have identified two main lively compounds out of this

extract: (1) myo-Inositol (MI) and (2)...

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