Decreased viability and absence-like epilepsy in mice lacking or deficient in the GABAA receptor α1 subunit
Author:
Publisher
Wiley
Subject
Neurology (clinical),Neurology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/j.1528-1167.2012.03596.x/fullpdf
Reference14 articles.
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2. Excitatory action of GABA on immature neurons is not due to absence of ketone bodies metabolites or other energy substrates;Ben-Ari;Epilepsia,2011
3. Absence epilepsy in apathetic, a spontaneous mutant mouse lacking the h channel subunit, HCN2;Chung;Neurobiol Dis,2009
4. Mutation of GABRA1 in an autosomal dominant form of juvenile myoclonic epilepsy;Cossette;Nat Genet,2002
5. The GABA-A receptor alpha 1 subunit mutation A322D associated with autosomal dominant juvenile myoclonic epilepsy reduces the expression and alters the composition of wild type GABA-A receptors;Ding;J Biol Chem,2010
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