GABA[subscript A] Receptor Downregulation in Brains of Subjects with Autism

Autor/inn/en	Fatemi, S. Hossein; Reutiman, Teri J.; Folsom, Timothy D.; Thuras, Paul D.
Titel	GABA[subscript A] Receptor Downregulation in Brains of Subjects with Autism
Quelle	In: Journal of Autism and Developmental Disorders, 39 (2009) 2, S.223-230 (8 Seiten) PDF als Volltext Verfügbarkeit
Sprache	englisch
Dokumenttyp	gedruckt; online; Zeitschriftenaufsatz
ISSN	0162-3257
DOI	10.1007/s10803-008-0646-7
Schlagwörter	Autism; Pathology; Brain; Cognitive Processes; Neurological Organization; Brain Hemisphere Functions; Seizures; Neurological Impairments + Suchen Sie Ihr Suchwort? Autismus; Pathologie; Gehirn; Cognitive process; Kognitiver Prozess; Anfallsleiden; Neurodegenerative Erkrankung
Abstract	Gamma-aminobutyric acid A (GABA[subscript A]) receptors are ligand-gated ion channels responsible for mediation of fast inhibitory action of GABA in the brain. Preliminary reports have demonstrated altered expression of GABA receptors in the brains of subjects with autism suggesting GABA/glutamate system dysregulation. We investigated the expression of four GABA[subscript A] receptor subunits and observed significant reductions in GABRA1, GABRA2, GABRA3, and GABRB3 in parietal cortex (Brodmann's Area 40 (BA40)), while GABRA1 and GABRB3 were significantly altered in cerebellum, and GABRA1 was significantly altered in superior frontal cortex (BA9). The presence of seizure disorder did not have a significant impact on GABA[subscript A] receptor subunit expression in the three brain areas. Our results demonstrate that GABA[subscript A] receptors are reduced in three brain regions that have previously been implicated in the pathogenesis of autism, suggesting widespread GABAergic dysfunction in the brains of subjects with autism. (As Provided).
Anmerkungen	Springer. 233 Spring Street, New York, NY 10013. Tel: 800-777-4643; Tel: 212-460-1500; Fax: 212-348-4505; e-mail: service-ny@springer.com; Web site: http://www.springerlink.com
Erfasst von	ERIC (Education Resources Information Center), Washington, DC
Update	2017/4/10