The Effect of Folic Acid on GABAA-B 1 Receptor Subunit
Autism contains a spectrum of behavioral and cognitive disturbances of childhood development that is manifested by deficits in social interaction, impaired communication, repetitive behavior, and/or restricted interest. Much research has been dedicated to finding the genes that are responsible for autism, but less than 10% of the cases can be attributed to one gene. Autism prevalence has increased in the last decade and there may be environmental components that are leading to this increase. There are reports of disruption of epigenetic mechanisms controlling the regulation of gene expression as probable cause for autism. Folic acid (FA) is prescribed to women during pregnancy, and can cause epigenetic changes. GABAergic pathway is involved in inhibitory neurotransmission in the central nervous system and plays a crucial role during early embryonic development. Autism may entail defect or deregulation of the GABAergic receptor pathway in the brain. Gamma-aminobutyric acid (type A) beta 1 receptor (GABRB1) disruption has been implicated in autism. In the present study, we investigated GABRB1 expression in response to FA supplementation in neuronal cells. Western blot analysis showed GABRB1 protein levels increased in the FA-treated cells in a concentration-dependent manner. FA-dependent increased expression of GABRB1 was further confirmed at the mRNA level using quantitative RT-PCR. These results suggest that epigenetic control of gene expression may affect the expression of GABRB1 and disrupt inhibitory synaptic transmission during embryonic development.
KeywordsPenicillin Glutamine Folic Acid Streptomycin Neuroblastoma
Gamma-aminobutyric acid type A receptor beta 1 subunit
Gamma-aminobutyric acid type A receptors
Glutamic acid decarboxylase
This study is supported by funds from the New York State Office for People with Developmental Disabilities, The City University of New York, The College of Staten Island, and Louis Stokes Alliance for Minority Participation a division of National Science Foundation (NSF). Financial assistance to Kizzy Vasquez is gratefully acknowledged.
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