GABAA-rho receptor
The GABAA-rho receptor (previously known as the GABAC receptor) is a subclass of GABAA receptors composed entirely of rho () subunits. GABAA receptors including those of the -subclass are ligand-gated ion channels responsible for mediating the effects of gamma-amino butyric acid (GABA), the major inhibitory neurotransmitter in the brain. The GABAA- receptor, like other GABAA receptors, is expressed in many areas of the brain, but in contrast to other GABAA receptors, the GABAA- receptor has especially high expression in the retina.

# Nomenclature
A second type of ionotropic GABA receptor, insensitive to typical allosteric modulators of GABAA receptor channels such as benzodiazepines and barbiturates, was designated GABA receptor. Native responses of the GABAC receptor type occur in retinal bipolar or horizontal cells across vertebrate species.
GABA receptors are exclusively composed of  (rho) subunits that are related to GABAA receptor subunits. Although the term "GABA receptor" is frequently used, GABA may be viewed as a variant within the GABAA receptor family. Others have argued that the differences between GABA and GABAA receptors are large enough to justify maintaining the distinction between these two subclasses of GABA receptors. However, since GABA receptors are closely related in sequence, structure, and function to GABAA receptors and since other GABAA receptors besides those containing  subunits appear to exhibit GABA pharmacology, the Nomenclature Committee of the IUPHAR has recommended that the GABA term no longer be used and these  receptors should be designated as the  subfamily of the GABAA receptors (GABAA-).

# Function
In addition to containing a GABA binding site, the GABAA- receptor complex conducts chloride ions across neuronal membranes. Binding of GABA to the receptor results in opening of this channel. When the reversal potential of chloride is less than the membrane potential, chloride ions flow down their electrochemical gradient into the cell. This influx of chloride ions lowers the membrane potential of the neuron, thus hyperpolarizes it, making it more difficult for these cells to conduct electrical impulses in the form of an action potential. Following stimulation by GABA, the chloride current produced by GABAA- 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 GABAA- than it is at most GABAA receptors.

# Structure
Like other ligand-gated ion channels, the GABAA- chloride channel is formed by oligomerization of five subunits arranged about a fivefold symmetry axis to form a central ion conducting pore. To date, three GABAA- receptor subunits have been identified in humans:
- 1 (GABRR1)
- 2 (GABRR2)
- 3 (GABRR3)
The above three subunits coassemble either to form functional homo-pentamers (15, 25, 35) or hetero-pentamers (1m2n, 2m3n where m + n = 5).
There is also evidence that 1 subunits can form hetero-pentameric complexes with GABAA receptor 2 subunits.

# Pharmacology
There are several pharmacological differences that distinguish GABAA- from GABAA and GABAB receptors. For example, GABAA- receptors are:
- selectively activated by (+)-CAMP  and blocked by TPMPA ;
- 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.

# Selective Ligands

## Agonists
- CACA
- CAMP
- GABOB

## Antagonists
- ZAPA ((Z)-3-prop-2-enoic acid)
- SKF-97541 (3-Aminopropyl(methyl)phosphinic acid)
- CGP-36742 (3-aminopropyl-n-butyl-phosphinic acid)
- TPMPA
- ()-cis-(3-Aminocyclopentyl)butylphosphinic acid
- (S)-(4-Aminocyclopent-1-enyl)butylphosphinic acid
- N2O

# Genetics
In humans, GABAA- receptor subunits 1 and 2 are encoded by the GABRR1 and GABRR2 genes which are found on chromosome 6 whereas the GABRR3 gene for 3 is found on chromosome 3 Mutations in the 1 or 2 genes may be responsible for some cases of autosomal recessive retinitis pigmentosa.