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The GABAC receptor is one of two ligand-gated ion channels responsible for mediating the effects of Gamma-Amino Butyric Acid (GABA), the major inhibitory neurotransmitter in the brain. The GABAC receptor, like the closely-related GABAA receptor, is expressed in many areas of the brain, but in contrast to GABAA, the GABAC receptor has especially high expression in the retina.
In addition to containing a GABA binding site, the GABAC receptor complex conducts chloride ions across neuronal membranes. Binding of GABA to the receptor results in opening of this channel, allowing chloride ions to flow down their electrochemical gradient into the cell. This increase in chloride current stabilizes the resting potential, making it more difficult for these cells conduct electrical impulses. Following stimulation by GABA, the chloride current produced by GABAC receptors is slow to initiate but sustained in duration. In contrast, the GABAA receptor current has a rapid onset and short duration. GABA is about 10 times more potent at GABAC than it is at most GABAA receptors.
Like other ligand-gated ion channels, the GABAC chloride channel is formed by oligomerization of five subunits arranged about a five-fold symmetry axis to form a central ion conducting pore. To date, three GABAC receptor subunits have been identified in humans:
- selectively activated by (+)-CAMP [(+)-cis-2-aminomethylcyclopropane-carboxylic acid] and blocked by TPMPA [(1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid];
- not sensitive to the GABAB agonist baclofen nor the GABAA receptor antagonist bicuculline;
- not modulated by many GABAA receptor modulators such as barbiturates, benzodiazepines, and neuroactive steroids.
In humans, GABAC receptor subunits ρ1 and ρ2 are encoded by the GABRR1 and GABRR2 genes which are found on chromosome 6 whereas the GABRR3 gene for ρ3 is found on chromosome 3. Mutations in the ρ1 or ρ2 genes may be responsible for some cases of autosomal recessive retinitis pigmentosa.
- ↑ Qian H. 2000. GABAc receptors in the vertebrate retina. Retrieved on February 14, 2007.
- ↑ 2.0 2.1 Martin IL and Dunn SMJ. GABA receptors A review of GABA and the receptors to which it binds. Tocris Cookson LTD.
- ↑ Enz R, Cutting GR (1998). Molecular composition of GABAC receptors. Vision Res 38 (10): 1431-41.
- ↑ Ogurusu T, Yanagi K, Watanabe M, Fukaya M, Shingai R (1999). Localization of GABA receptor rho 2 and rho 3 subunits in rat brain and functional expression of homo-oligomeric rho 3 receptors and hetero-oligomeric rho 2 rho 3 receptors. Receptors Channels 6 (6): 463-75.
- ↑ Chebib M, Johnston GA (2000). GABA-Activated ligand gated ion channels: medicinal chemistry and molecular biology. J Med Chem 43 (8): 1427-47.
- ↑ Marcos I, Ruiz A, Blaschak CJ, Borrego S, Cutting GR, Antinolo G (1998). Mutation analysis of GABRR1 and GABRR2 in autosomal recessive retinitis pigmentosa. J Med Genet 37 (6): E5.
Ion channel, receptor: ligand-gated ion channels
5-HT receptor (5-HT3 serotonin receptor (A)) - GABA receptor (GABA A (α1, α2, α3, α4, α5, α6, β1, β2, β3, γ2, γ3, ε), GABA C (ρ1, ρ2)) - Glycine receptor (α1, α2, β) - Nicotinic acetylcholine receptor (α1, α2, α3, α4, α5, α7, α9, β1, β2, β3, β4, δ, ε, (α4)2(β2)3, (α7)5, Ganglion type, Muscle type)
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