Nomenclature: γ2

Family: GABAA receptors

Annotation status:  image of a green circle Annotated and expert reviewed. Please contact us if you can help with updates. 

Contents

Gene and Protein Information
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 4 475 5q31.1-q33.1 GABRG2 gamma-aminobutyric acid (GABA) A receptor, gamma 2 25,39
Mouse 4 474 11 A5 Gabrg2 gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2 37
Rat 4 466 10q21 Gabrg2 gamma-aminobutyric acid (GABA) A receptor, gamma 2 28
Previous and Unofficial Names
CAE2
ECA2
GEFSP3
Gabrg-2
RP23-227J8.1
AI851231
BB128510
gamma2
GABA(A) receptor, gamma 2
GABA(A) receptor subunit gamma-2
gamma-aminobutyric acid (GABA-A) receptor subunit gamma 2
gamma-aminobutyric acid (GABA-A) receptor, subunit gamma 2
gamma-aminobutyric acid A receptor, gamma 2
gamma-aminobutyric acid receptor subunit gamma-2
GABAA-R
Database Links
ChEMBL Target
Ensembl Gene
Entrez Gene
GeneCards
GenitoUrinary Development Molecular Anatomy Project
HomoloGene
Human Protein Reference Database
InterPro
KEGG Gene
OMIM
Orphanet Gene
PharmGKB Gene
PhosphoSitePlus
Protein Ontology (PRO)
RefSeq Nucleotide
RefSeq Protein
TreeFam
UniGene Hs.
UniProtKB
Wikipedia
Natural/Endogenous Ligands
GABA
Channel Blockers
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Use-dependent Affinity Units Concentration range (M) Voltage-dependent (mV) Reference
TBPS Hs - no - - - no

Not voltage dependent
picrotoxin ? - no - - - no

Not voltage dependent
View species-specific channel blocker tables
Tissue Distribution
Olfactory bulb (granule cells), tenia tecta, thalamus (medio dorsal, dorsolateral geniculate, ventrolateral geniculate, ventral posterior nucleus)
Expression level:  Low
Species:  Rat
Technique:  In situ hybridisation
References:  23,40
Olfactory bulb (mitral cells), pyriform cortex, hippocampus (CA1, CA3, dentate gyrus), erebellum (Purkinje cells)
Expression level:  High
Species:  Rat
Technique:  In situ hybridisation
References:  40
Olfactory bulb (periglomerular and tufted cells), neocortex (layers II/III, IV, and V/IV), basal nuclei (caudate putamen, nucleus accumbens, globus pallidus, endopeduncular nucleus, claustrum, subthalamic nucleus), amygdala (central medial and lateral amgdaloid nucleus), septum (bed nuleus of stria terminalis, lateral and medial septum, diagonal band), medial habenula, thalamus (paraventricular and rhomboid nucleus, medial geniculate nucleus, parafascicular nucleus, zona incerta), hypothalamus (medial preoptic area, arcuate nucleus, dorsomedial nucleus, ventromedial nucleus), midbrain (red nucleus), inferior colliculi (central nucleus), substantia nigra (pars reticulata, pars compacta), cerebellum (stellate, basket and granule cells)
Expression level:  Medium
Species:  Rat
Technique:  In situ hybridisation
References:  23,40
The γ2 subunit is part on average of at least 80% of all GABA(A) receptors in virtually all neurons across all brain regions including the olfactory system, cerebral cortex, hippocampus, dentate gyrus, amygdala, septal and basal forebrain, cerebral nuclei, thalamus, hypothalamus, midbrain and pons, medulla, cranial nerve nuclei, cerebellum
Expression level:  High
Species:  Rat
Technique:  In situ hybridisation
References:  11,24
Tissue Distribution Comments
The data tabulated for the human and mouse γ2 subunits correspond to transcript variant 1 encoding the variant commonly referred to as γ2L. The data tabulated for rat correspond to transcript variant 2 encoding a shorter version of γ2 (γ2S, 466 amino acid residues) that lacks eight amino acids in the M3-M4 cytoplamic loop region.
Physiological Consequences of Altering Gene Expression
Heterozygous deletion of the γ2 subunit in mice results in elevated trait anxiety and altered emotional behavior reminiscent of melancholic depression. This phenotype includes increased behavioral sensitivity to diazepam, enhanced trace conditioning and deficits in ambiguous cue discrimination learning but unaltered delay conditioning, context conditioning and spatial learning (Crestani et al., 1999). The γ2+/- model includes reduced survival of adult-born hippocampal neurons, increased behavioral passivity in the forced swim and tail suspension tests (Earnheart et al., 2007), depression related anhedonia in the sucrose consumption test, as well as constitutively elevated serum corticosterone levels (Shen et al., 2010). The anxiety- like but not the depression-related behavior in the forced swim, tail suspension and sucrose consumption tests are reversed with fluoxetine. By contrast, chronic treatment with the tricyclic antidepressant desipramine reverses anxiety and depression related behavior in all four tests and also normalizes HPA axis function (Shen et al., 2010). Conditional deletion of the γ2 subunt indicates that HPA axis dysfunction is independent of a GABA(A) receptor deficit in the hypothalamus. Moreover, γ2-deficit-induced HPA axis dysfunction is insufficient to induce anxiety and depression-related behavior of γ2+/- mice (Shen et al., 2010)
Species:  Mouse
Tissue: 
Technique:  Heteroygous knockout, forebrain glutamatergc neuron-specific heterozygous knockout, developmental stage- specific knockout
References:  7,9,29
Knockout of the γ2 subunit results in loss of 94% of [3H] flumazenil binding sites and loss of 22% of GABA ([3H]SR 95531) binding sites. It is asociated with perinatal lethality with very few mice surviving to maximally the 3rd postnatal week (Gunther et al., 1995). GABA-evoked whole cell currents of dorsal root ganglia neurons are reduced to approx 37% of wildtype controls (Gunther et al., 1995). Loss of the γ2 subunit results in loss of postsynaptic GABA(A) receptors and the subsynaptic scafold protein gephyrin from virtually all GABAergic synapses. Functionally this is reflected in virtually complete loss of GABAergic miniature inhibitory synaptic currents (mIPSCs) (Essrich et al., 1998; Schweizer et al., 2003; Alldred et al., 2005). Similar functional deficits in GABAergic synapses are observed upon cell type-specific knockout of the γ2 subunit (Wulff et al., 2009, 2010).
Species:  Mouse
Tissue:  Brain, dorsal root ganglia, cortical neuron cultures
Technique:  Knockout
References:  1,10,12,27,41-42
shRNA mediated knock down of γ2 mRNA results in reduced GABAergic innervation of pyramidal cells
Species:  Rat
Tissue:  Brain, cultured hippoxampal neurons
Technique:  shRNA mediated knockdown
References:  18
Conditional homozygous deletion of the γ2 subunit in glutamatergic neurons of the forebrain in the 4th-5th postnatal week results in a lethal epilepsy phenotype (Schweizer et al., 2003).
Species:  Mouse
Tissue:  Forebrain
Technique:  Cre-loxP, CaMKII-Cre mediated recombination
References:  27
A mouse model of the human R82Q mutation (R43Q in the mature peptide), which is associated with familial childhood absence epilepsy (CAE-2), shows behavioral arrest associated with 6-to 7-Hz spike-and-wave discharges, which are blocked by ethosuximide. Mice that are homozygous for the corresponding mutation show a perinatally lethal phenotype comparable to that of γ2 KO mice
Species:  Mouse
Tissue: 
Technique:  Knock-in
References:  33
Global elimination of the Y365/367 tyrosine phosphorylation site in the major cytoplasmic loop region of the γ2 subunit (Y365/367F) results in reduced endocytosis and increased accumulation of γ2-containing GABA(A) receptors at inhibitory synapses selectively on pyramidal cells of the hippocampal CA3 region. Behaviorally, the mice show impaired spatial object recognition.
Species:  Mouse
Tissue: 
Technique:  Knock-in γ2
References:  34
Transgenic expression of the γ2S or γ2L subunit under control of the human beta actin gene promoter in a γ2 knockout (perinatally lethal) background is sufficient to restore postsynaptic clustering and inhibitory synaptic function of GABA(A) receptors, leading to viable mice without an overt behavioral phenotype
Species:  Mouse
Tissue: 
Technique:  Transgenic expression, knockout
References:  3
Clinically-Relevant Mutations and Pathophysiology
Disease:  Severe myoclonic epilepsy in infancy, SMEI
OMIM:  607208
Orphanet:  33069
Role: 
References:  6,22,43
Click column headers to sort
Type Species Molecular location Description Reference
Truncation Human Q390X 13
Truncation Human Q40X (first amino acid of mature peptide) 14
Disease:  Epilepsy, Childhood Absence, susceptibility to, 2; ECA2
OMIM:  607681
Orphanet:  64280
Role: 
Side effects:  Generalized tonic-clonic seizures often develop in adolescence
References:  8
Click column headers to sort
Type Species Molecular location Description Reference
Missense Human R82Q 20,36
Other Human GT->GG Splice donor site in intron 6 16
Disease:  Febrile Convulsions, Familial 8, FEB8
OMIM:  611277
Orphanet:  36387
Role: 
References:  20-21,36
Click column headers to sort
Type Species Molecular location Description Reference
Missense Human R82Q 20,36
Missense Human R177G 2
Other Human GT->GG Splice donor site in intron 6 16
Disease:  Generalized Epilepsy with Febrile Seizures Plus; GEFS+
OMIM:  611277
Orphanet:  36387
Role: 
References:  26,31
Click column headers to sort
Type Species Molecular location Description Reference
Missense Human K328M 4
Truncation Human Q390X 13
Truncation Human Q429X 32
Clinically-Relevant Mutations and Pathophysiology Comments
Amino acid numbers tabulated refer to full-length precursor proteins encoded by transcript variant 1. Thus, K328M corresponds to K289M, R82Q corresponds to R43Q. R177G correponds to R138G (mislabeled as R139G in Ohmori et al., 2002 [22]) of the mature protein.
Biologically Significant Variants
Type:  Splice variant
Species:  Human
Description:  Transcript variant 1 encoding γ2L
Amino acids:  475
Nucleotide accession: 
Protein accession: 
References:  15,25
Type:  Splice variant
Species:  Human
Description:  Transcript variant 2, encodes a γ2S subunit lacking 8 amino acid in the M3-M4 cytoplasmic loop region compared to γ2L
Amino acids:  467
Nucleotide accession: 
Protein accession: 
References:  15,25
Type:  Splice variant
Species:  Human
Description:  Transcript variant 3, encodes an alternatively spliced version of the γ2 subunit with an additional 40 amino acids in the extracellular domain compared to transcript variants 1 and 2.
Amino acids:  515
Nucleotide accession: 
Protein accession: 
References:  15,25
Type:  Splice variant
Species:  Rat
Description:  Transcript variant 2, encodes a γ2S subunit lacking 8 amino acid in the M3-M4 cytoplasmic loop region compared to γ2L
Amino acids:  466
Nucleotide accession: 
Protein accession: 
References:  19,30,35
Type:  Splice variant
Species:  Mouse
Description:  Transcript variant 1 encoding γ2L
Amino acids:  474
Nucleotide accession: 
Protein accession: 
References:  5
Type:  Splice variant
Species:  Mouse
Description:  Transcript variant 2, encodes the γ2S subunit lacking 8 amino acid in the M3-M4 cytoplasmic loop region compared to γ2L
Amino acids:  466
Nucleotide accession: 
Protein accession: 
References:  5,17
Biologically Significant Variant Comments
A transcript variant 1 of the rat Gabrg2 gene is not currently available in the rat genome database. However, the 24bp acid exon that distinguishes mouse and human transcript variant 1 from transcript variant 2 (encoding LLRMFSFK) is conserved in the rat genomic sequence NM_183327. Transcript variants 1 and 2 are further available for the bovine gene [38].

REFERENCES

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To cite this database page, please use the following:

Bernhard Luscher.
GABAA receptors: γ2. Last modified on 14/03/2014. Accessed on 01/08/2014. IUPHAR database (IUPHAR-DB), http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=414.

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