Preview

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

Powerful Essays
Open Document
Open Document
6110 Words
Grammar
Grammar
Plagiarism
Plagiarism
Writing
Writing
Score
Score
Myo-Inositol Treatment and Gaba-a Receptor Subunit Changes After Kainate- Induced Status Epilepticus
123
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
Your article is protected by copyright and all rights are held exclusively by Springer
Science+Business Media, LLC. This e-offprint is for personal use only and shall not be selfarchived in electronic repositories. If you wish to self-archive your work, please use the accepted author’s version for posting to your own website or your institution’s repository.
You may further deposit the accepted author’s version on a funder’s repository at a funder’s request, provided it is not made publicly available until 12 months after publication.
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



References: Alldred MJ, Mulder-Rosi J, Lingenfelter SE, Chen G, Luscher B (2005) Distinct gamma2 subunit domains mediateclustering and Bencsits E, Ebert V, Tretter V, Sieghart W (1999) A significant part of native gamma-aminobutyric acid A receptors containing Brooks-Kayal AR, Raol YH, Russek SL (2009) Alteration of epileptogenesis genes Browne TR, Holmes GL (2001) Epilepsy. N Engl J Med 344:1145–1151 Choi DW (1987) Ionic dependence of glutamate neurotoxicity. J Neurosci 7:369–379 Clement AB, Hawkins A, Lichtman AH, Cravatt BF (2003) Increased 23:3916–3923 De Blas AL (1996) Brain GABAA receptors studied with subunit specific antibodies. Mol Neurobiol 12:55–71 Dietzel I, Heinenmann U, Hofinier G, Lux HD (1982) Stimulusinduced Res 46:73–84 Dittmer A, Dittmer J (2006) Beta-actin is not a reliable loading control in western blot analysis. Electrophoresis 27:2844–2845 Dudek FE, Obenaus A, Tasker JG (1990) Osmolality induced changes Essrich C, Lorez M, Benson JA, Fritschy JM, Luscher B (1998) Postsynaptic clustering of major GABAA receptor subtypes Fisher KS, Novak JE, Agranoff BW (2002) Inositol and higher inositol phosphates in neuronal tissues: homeostasis, metabolism Moshe SL, Zukin RS (1994) Kainate-induced status epilepticus alters glutamate and GABA-A receptor gene expression in adult Gonzalez MI, Brooks-Kayal A (2011) Altered GABA-A receptor expression during epileptogenesis Jia F, Pignataro S, Schofield CM, Yue M, Harrison NL, Goldstein PA (2005) An extrasynaptic GABAA receptor mediates tonic Joshi S, Kapur J (2009) Slow intracellular accumulation of GABA(A) receptor delta subunit is modulated by brain-derived B, Miller ER, Kelly KM, Mtchedlishvili Z (2011) Alterations of GABA(A) and glutamate receptor subunits and heat shock Loescher W, Gernert M, Heinemann U (2008) Cell and gene therapies in epilepsy–promising avenues or blind alleys? Trends Neurosci 31:62–73 Macdonald RL, Kang JQ, Gallagher MJ (2010) Mutations in GABAA Majores M, Schoch S, Lie A, Becker AJ (2007) Molecular neuropathology of temporal lobe epilepsy: complementary Mangan PS, Sun C, Carpenter M, Goodkin HP, Sieghart HP, Kapur J (2005) Cultured hippocampal pyramidal neurons express two kinds of GABAA receptors. Mol Pharmacol 67:775–788 McNamara JO, Huang YZ, Leonard AS (2006) Molecular signaling Nozadze M, Mikautadze M, Lepsveridze E, Mikeladze E, Kuchiashvili N, Kiguradze T, Kikvidze M, Solomonia R (2011) 20:173–176 Nusser Z, Mody I (2002) Selective modulation of tonic and phasic Olsen RW, Sieghart W (2009) GABAA receptors: subtypes provide diversity of function and pharmacology Walker MC (2011) Progressive loss of phasic, but not tonic GABA-A receptor-mediated inhibition in dentate granule cells in Racine RJ (1972) Modification of seizure activity by electrical stimulation II 32:281–294 Rothman SM (1985) The neurotoxicity of excitatory amino acid is produced by passive chloride influx. J Neurosci 5:1483–1489 Rowley NM, Smith MD, Lamb JG, Schousboe A, White S (2011) 117:82–90 Schwartzkoin PA, Baraban SC, Hochmann DW (1998) Osmolarity,

You May Also Find These Documents Helpful