All Relations between Epilepsy and gaba

Reference Sentence Publish Date Extraction Date Species
Sara Olivotto, Anna Freddi, Rossella Lavatelli, Eleonora Basso, Alessia Leidi, Barbara Castellotti, Luigina Spaccini, Stefania Maria Bova, Pierangelo Veggiott. Successful use of perampanel in GABRA1-related myoclonic epilepsy with photosensitivity. Epilepsy & behavior reports vol 19 issue 2022 35520951 pathogenic variants in gamma-aminobutyric acid type a receptor subunit alpha1 (gabra1) is a protein coding gene that has been associated with a broad phenotypic spectrum of epilepsies. 2022-05-06 2022-05-07 Not clear
Svetlana Gataullina, Thierry Bienvenu, Rima Nabbout, Gilles Huberfeld, Olivier Dula. Gene mutations in paediatric epilepsies cause NMDA-pathy, and phasic and tonic GABA-pathy. Developmental medicine and child neurology vol 61 issue 8 2019 30680721 three mechanisms are shared by most monogenic epilepsies: (1) excess of n-methyl-d-aspartate (nmda) transmission activation (nmda-pathies); (2)\xc2\xa0abnormal gamma-aminobutyric acid (gaba) transmission with reduced inhibition (phasic gaba-pathies); and (3) tonic activation of extrasynaptic gaba 2019-11-28 2022-01-13 Not clear
Jeffrey Britto. Autoimmune epilepsy. Handbook of clinical neurology vol 133 issue 2017 27112680 first, epilepsies secondary to other primary autoimmune disorders will be discussed, and then those associated with antibodies that are likely to be pathogenic, such as voltage-gated potassium channel-complex and n-methyl-d-aspartate receptor, gamma-aminobutyric acid a and b receptor antibodies. 2017-02-09 2022-01-12 Not clear
Roman Tyzio, Ilgam Khalilov, Alfonso Represa, Valerie Crepel, Yuri Zilberter, Sylvain Rheims, Laurent Aniksztejn, Rosa Cossart, Romain Nardou, Marat Mukhtarov, Marat Minlebaev, J\\xc3\\xa9r\\xc3\\xb4me Epsztein, Mathieu Milh, Helene Becq, Isabel Jorquera, Christine Bulteau, Martine Fohlen, Viviana Oliver, Olivier Dulac, Georg Dorfm\\xc3\\xbcller, Olivier Delalande, Yehezkel Ben-Ari, Roustem Khazipo. Inhibitory actions of the gamma-aminobutyric acid in pediatric Sturge-Weber syndrome. Annals of neurology vol 66 issue 2 2009 19743469 we explored the properties of neurons from human pediatric sws cortex in vitro and tested in particular whether gamma-aminobutyric acid (gaba) excites neurons in sws cortex, as has been suggested for various types of epilepsies. 2009-10-01 2022-01-12 Not clear
Yehezkel Ben-Ari, Gregory L Holme. The multiple facets of gamma-aminobutyric acid dysfunction in epilepsy. Current opinion in neurology vol 18 issue 2 2005 15791144 the polarity of action of gamma-aminobutyric acid (gaba) changes from inhibition to excitation in the developing brain and in epilepsies. 2005-06-13 2022-01-12 Not clear
Feyza Sancar, Cynthia Czajkowsk. A GABAA receptor mutation linked to human epilepsy (gamma2R43Q) impairs cell surface expression of alphabetagamma receptors. The Journal of biological chemistry vol 279 issue 45 2004 15342642 a mutation in the gamma2 subunit of the gamma-aminobutyric acid (gaba) type a receptor (gabar), which changes an arginine to a glutamine at position 43 (r43q), is linked to familial idiopathic epilepsies. 2004-12-28 2022-01-12 Not clear
E Mesdjian, L Ciesielski, P Mande. GABAA sodium independent receptor sites in a strain of rats presenting generalized non-convulsive seizures. Neuroscience letters vol 136 issue 2 1992 1322518 the role of gamma-aminobutyric acid (gaba), a major inhibitor neurotransmitter in the central nervous system (cns), is well established in the genesis and the control of epilepsies. 1992-08-28 2022-01-10 Not clear
R Agosti, G Yasargil, M Egli, H G Wieser, O D Wiestle. Neuropathology of a human hippocampus following long-term treatment with vigabatrin: lack of microvacuoles. Epilepsy research vol 6 issue 2 1990 2387287 vigabatrin (gamma-vinyl-gaba), an irreversible inhibitor of gamma-aminobutyric acid transaminase, has been reported to be effective in the treatment of refractory epilepsies. 1990-09-25 2022-01-10 Not clear
A V Delgado-Escueta, D Greenber. The search for epilepsies ideal for clinical and molecular genetic studies. Annals of neurology vol 16 Suppl issue 1984 6095735 an approach more likely to succeed is to use as markers the dna fragments of proteins that are suspected to cause the disease in experimental models of genetic epilepsies; for example, the gamma-aminobutyric acid receptor genes, which are suspected to cause myoclonic epilepsy in experimental animals, can be tested in benign juvenile myoclonic epilepsy. 1984-12-26 2022-01-10 Not clear
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