GABA receptor: Difference between revisions
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== Disease == | == Disease == | ||
[[Image:GABAB receptor 1.gif|right|350px]] | [[Image:GABAB receptor 1.gif|right|350px]] | ||
GABAB receptors are targeted for a number of treatments in the clinical setting of neurodegenerative and pathophysiolocial disorders including epilepsy, spasticity, chronic pain, anxiety, depression, schizophrenia, cognitive function, gastro-esophageal reflux and drug dependence and addition (Kerr 2005). | |||
There is increasing evidence that links schizophrenia directly to GABAB receptor deficits. GABBR1, the gene associated with the GABAB1 receptor was found to have a high number of differentially methylated CpGs, or hyper methylation in receptors tested for patients with schizophrenia (Citrine et al. 2009). The receptor 1 gene is on chromosome 6 where the locus is susceptible for multiple sclerosis, epilepsy, and schizophrenia (Sigma Aldrich). Presynaptic dopaminergic terminals have GABAB receptors that are involved in the release of dopamine along with modulation of glutaminergic regulation of dopamine (Citrome et al. 2009). | |||
A possible therapeutic approach utilizing GABAB receptors would be for the treatment substance use disorder (drug addition). Since the GABAB receptor plays a crucial role in mediating behavioral and molecular effects of drug abuse, the GABAB receptor can be utilized as a potential anti-addictive therapeutic strategy (Flip et. al, 2015). Agonists at GABAB receptors can promote abstinence or decrease and control the reinforcing effects of drugs on the mind (Kerr 2005). | |||
== References == | == References == | ||
