GABAA receptor α3 subunit

Target id: 406

Nomenclature: GABAA receptor α3 subunit

Family: GABAA receptors

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

   GtoImmuPdb view: OFF :     Currently no data for GABAA receptor α3 subunit in GtoImmuPdb

Gene and Protein Information
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 4 492 Xq28 GABRA3 gamma-aminobutyric acid type A receptor alpha3 subunit 5,15
Mouse 4 492 X A7.3 Gabra3 gamma-aminobutyric acid (GABA) A receptor, subunit alpha 3 17
Rat 4 493 Xq37 Gabra3 gamma-aminobutyric acid type A receptor alpha3 subunit 42
Previous and Unofficial Names
gamma-aminobutyric acid receptor subunit alpha-3
Gabra-3
gamma-aminobutyric acid (GABA) A receptor, alpha 3
Database Links
ChEMBL Target
DrugBank Target
Ensembl Gene
Entrez Gene
GenitoUrinary Development Molecular Anatomy Project
KEGG Gene
OMIM
Orphanet
RefSeq Nucleotide
RefSeq Protein
UniProtKB
Wikipedia
Associated Proteins
Heteromeric Pore-forming Subunits
Name References
GABAA receptor β3 subunit
GABAA receptor γ2 subunit
Auxiliary Subunits
Name References
Not determined
Other Associated Proteins
Name References
Not determined
Associated Protein Comments
Heteromeric GABAA receptors can be formed from the proteins listed in the table above. These receptors generally consist of 2 α, 2 β and 1 γ subunit. An example of GABAA receptors containing the α3 subunit include α3β3γ2.
Natural/Endogenous Ligands
GABA

Download all structure-activity data for this target as a CSV file

Agonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Affinity Units Reference
CGS8216 Hs Inverse agonist 9.9 pKi 18
pKi 9.9 (Ki 1.2x10-10 M) [18]
ZK93423 Hs Full agonist 8.4 pKi 6
pKi 8.4 (Ki 4.5x10-9 M) [6]
[3H]muscimol Hs Agonist - -
[Binds to: GABA site]
isoguvacine Hs Full agonist - -
[Binds to: GABA site]
isonipecotic acid Hs Agonist - -
[Binds to: GABA site]
muscimol Hs Full agonist - -
[Binds to: GABA site]
piperidine-4-sulphonic acid Hs Full agonist - -
[Binds to: GABA site]
gaboxadol Hs Agonist - -
[Binds to: GABA site]
Antagonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Affinity Units Reference
bicuculline Hs Antagonist - -
[Binds to: GABA site]
[3H]gabazine Hs Antagonist - -
[Binds to: GABA site]
gabazine Hs Antagonist - -
[Binds to: GABA site]
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
picrotoxin Hs - no - - - no

Not voltage dependent
TBPS Hs - no - - - no

Not voltage dependent
[35S]TBPS Hs - no - - - no
[Binds to: anion channel]
Not voltage dependent
Allosteric Modulators
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Affinity Units Concentration range (M) Voltage-dependent (mV) Reference
flumazenil Hs Antagonist 9.0 pKi - no 19
pKi 9.0 (Ki 1.05x10-9 M) [Binds to: benzodiazepine site] [19]
Not voltage dependent
Description: Affinity measured using α3β3γ2 receptors.
AZD7325 Hs Positive 8.9 pKi - no 2
pKi 8.9 (Ki 1.3x10-9 M) [2]
Not voltage dependent
triazolam Hs Positive 8.8 pKi - no 18
pKi 8.8 (Ki 1.43x10-9 M) [18]
Not voltage dependent
Description: Binding affinity to human recombinant GABAA receptor α3β3γ2.
clonazepam Hs Positive 8.7 pKi - no 37
pKi 8.7 (Ki 2x10-9 M) [37]
Not voltage dependent
Description: Assay using recombinant GABAA channels with subunit composition; α3β1γ2.
flunitrazepam Hs Positive 7.8 pKi - no 14
pKi 7.8 (Ki 1.57x10-8 M) [Binds to: benzodiazepine site] [14]
Not voltage dependent
Description: Assay using recombinant GABAA channels with subunit composition; α3β1γ2.
diazepam Hs Positive 7.8 pKi - no 37
pKi 7.8 (Ki 1.7x10-8 M) [Binds to: benzodiazepine site] [37]
Not voltage dependent
Description: Assay using recombinant GABAA channels with subunit composition; α3β1γ2.
zolpidem Hs Positive 5.7 pKi - no 15
pKi 5.7 (Ki 2.15x10-6 M) [15]
Not voltage dependent
Description: Assay using recombinant GABAA channels with subunit composition; α3β1γ2.
alprazolam Hs Positive 7.2 pEC50 - no 1
pEC50 7.2 (EC50 6.9x10-8 M) [Binds to: benzodiazepine site] [1]
Not voltage dependent
Zn2+ Hs Inhibition - - - no

Not voltage dependent
α3IA Hs - - - - no
[Binds to: benzodiazepine site] higher affinity
Not voltage dependent
α5IA Hs Inverse agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
5α-pregnan-3α-ol-20-one Hs Potentiation - - - no

Not voltage dependent
bretazenil Hs Full agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
DMCM Hs Inverse agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
L838417 Hs Partial agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
MRK016 Hs Inverse agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
ocinaplon Hs Partial agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
Ro15-4513 Hs Inverse agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
Ro19-4603 Hs Inverse agonist - - - no
[Binds to: benzodiazepine site] higher affinity
Not voltage dependent
RO4938581 Hs Inverse agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
tetrahydrodeoxycorticosterone Hs Potentiation - - - no

Not voltage dependent
TP003 Hs Partial agonist - - - no
[Binds to: benzodiazepine site] high efficacy
Not voltage dependent
TPA023 Hs Partial agonist - - - no
[Binds to: benzodiazepine site] low efficacy
Not voltage dependent
ZK93426 Hs Antagonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
[3H]flunitrazepam Hs Full agonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
[3H]CGS8216 Hs Mixed - - - no
[Binds to: benzodiazepine site] agonist and antagonist
Not voltage dependent
[11C]flumazenil Hs Antagonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
[18F]fluoroethylflumazenil Hs Antagonist - - - no
[Binds to: benzodiazepine site]
Not voltage dependent
Allosteric Modulator Comments
Alprazolam is an approved drug which is a positive allosteric modulator of the GABAA receptor. It has affinity for the benzodizepine site on several α subunits.
Triazolam binds to the benzodiazepine binding site of the heteromeric GABAA receptor, binding at the extracellular interface between the α and γ subunits [43]. The drug has been mapped to the relevant, experimental α subunit, and heteromeric partners are listed in the Associated Proteins table above .
Tissue Distribution
Olfactory system (internal granular layer, anterior olfactory nucleus, olfactory tubercle), neocortex (layer 1, layers 2/3, layer 4), piriform cortex (layer 2), subiculum, presubiculum, hippocampus (CA1 stratum oriens and radiatum, CA3 stratum pyramidale, CA3 stratum oriens and radiatum), dentate gyrus (molecular layer), amgygdala (anterior amygdaloid area, central nucleus medial part, basomedial nucleus posterior part, lateral nucleus, medial nucleus, posterior cortical nucleus), lateral septal nucleus intermediate part, caudatoputamen (striatum), nucleus accumbens, globus pallidus, ventral pallidum, entopeduncular nucleus, thalamus (anteroventral nucleus, ventral medial nucleus, centromedial nucleus, parafascicular nucleus), epithalamus (lateral habenular nucleus), subthalamus (subthalamic nucleus), hypothalamus (medial preoptic area, anterio preoptic area, anterior hypothalamic area, lateral hypothalamic area, suprachiasmatic nucleus, paracentricular hypothalamic nucleus ventral part, paracentricular hypothalamic nucleus lateral magnocellular part, paracentricular hypothalamic medial parvocellular part, periventricular nucleus, retrochiasmatic area, tuber cireneum area, ventromedial nucleus, dorsomedial nucleus, posterior hypothalamic area), midbrain and pons (red nucleus parvocellular part, red nucleus macrocellular part, superior colloculus zonal layer, inferior colliculus external and dorsal cortex, intermediate nucleus of the lateral lemniscus, ventral nucleus of the lateral lemniscus, Koelliker-Fuse nucleus, dorsomedial tegmental nucleus, parbrachial nucleus), cranial nerve nuclei (oculomotor trochlear nuclei, motor trigeminal nucleus, facial nucleus, ambiguus nucleus, dorsal motor nucleus of the vagus, hypoglossus nucleus, trigeminal sensory complex mesencephalic trigeminal nucleus, cochlea nuclei ventral nucleus granular layer, solitary tract nucleus), cerebellum (cerebellar nuclei)
Expression level:  Low
Species:  Rat
Technique:  Immunohistochemistry.
References:  12,36
Basal nuclei (claustrum)
Expression level:  High
Species:  Rat
Technique:  In situ hybridisation
References:  35,49
Spinal cord. In situ hybridization for the α3 subunit indicates its expression in spinal cord layers II-VII and X. the labeling of motoneurons, however is extremely weak.
Species:  Rat
Technique:  In situ hybridisation
References:  34,48
Hippocampus. The α3 subunit is the least expressed α subunit in the hippocampus. In acetone fixed sections faint staining was detected in the inner molecular layer of the dentate gyrus, in CA3 and in the stratum lacunosum moleculare. In sections obtained from paraformaldehyde-perfused brains, faint (but specific) staining was also observed within principal cells.
Species:  Rat
Technique:  Immunohistochemistry.
References:  45
Spinal cord. Widespread distribution of α3 subunit in the spinal cord. Intense labeling of the superfical layer of the dorsal horn (lamina I-III). In the deep dorsal horn, intermediate zone and most of the ventral horn (lamina IV-VIII) a moderate to strong staining is observed for α3 subunits. These subunits were not detected in somatic and preganglionic motoneurons.
Species:  Rat
Technique:  Immunohistochemistry.
References:  3
Basal ganglia and limbic brain areas. In the substantia nigra pars compacta and in the ventral tegmental area numerous presumably dopaminergic neurons are labeled for α3. In the striatum, nucleus accumbens, and olfactory tubercle, globus pallidus, staining for α3 is light to moderate.
Species:  Rat
Technique:  Immunohistochemistry.
References:  41
Relatively strong neuropil and soma staining in cerebral cortex, especially in layer VI. Relatively weak staining throughout the hippocampus formation, but staining pattern in the CA1 sector was complementary to that observed for α2. No granule or pyramidal cell layer staining. Intense neuropil labeling in the reticular nucleus of the thalamus.
Species:  Rat
Technique:  Immunohistochemistry.
References:  51
Olfactory system (glomerulus, external plexiform layer, accessory olfactory bulb, islands of Calleja), neocortex (layer 6), insular cortex, perirhinal cortex, entorhinal cortex, endopiriform nucleus, parasubiculum, tenia tecta, amygdala (basomedial nucleus anterior part, basolateral nucleus, basolateral nucleus ventral part, intercalated nuclei), lateral septal nucleus dorsal and ventral parts, claustrum, thalamus (reticular nucleus, centrolateral nucleus, rhomboid nucleus), midbrain and pons (substantia nigra pars compacta, locus coeruleus, nucleus of the trapezoid body), medulla (gigantocellular reticular nucleus alpha part, raphe obscurus nucleus, inferior olivary complex medial nucleus), cranial nerve nuclei (trigenimal sensory complex principal nucleus, trigeminal sensory complex spinal nucleus pars oralis, trigeminal sensory complex spinal nucleus interpolar part, spinal nucleus caudal part layers 2-5. cochlear nuclei ventral nucleus)
Expression level:  High
Species:  Rat
Technique:  Immunohistochemistry
References:  12,36
Neocortex (layer V/VI), pyriform cortex, septum (bed nucleus of the stria terminalis, lateral septum), thalamus (rhomboid nucleus)
Expression level:  Medium
Species:  Rat
Technique:  In situ hybridisation
References:  35,49
Olfactoray bulb (periglomerular, tufted cells, mitra cells, granule cells), neocortex (layer II/III, layer IV), hippocampus (CA1 stratum pyramidalis, CA3 stratum pyramidalis), basal nuclei (caudate-putamen, nucleus accumbens, globus pallidus), amydgala (central amygdaloid nucleus, medial amygdaloid nucleus, lateral amygdaloid nucleus), septum (medial septum, diagonal band), medial habenula, thalamus (paraventricular nucleus, parafscicular nucleus, reticular nucleus, zona incerta), hypothalamus (medial preoptic area, dorsomedial nucleus, ventromedial nucleus, inferior colloculi (central nucleus), substantia nigra (pars reticulata, pars compacta), cerebellum (stellate/basket cells)
Expression level:  Low
Species:  Rat
Technique:  In situ hybridisation
References:  35,49
Olfactory system (mitral cell layer, nucleus of the lateral olfactory tract), neocortex (layer 5), piriform cortex (layers 1 and 3), dentate gyrus (hilus), amygdala (anterior cortical nucleus, central nucleus lateral part, amygdalohippocampal area), septohippocampal nucleus, medial septal nucleus, nucleus of the diagonal band, substantia innominata magnocellular preoptic nucleus, bed nucleus of the stria terminalis, thalamus (paraventricular thalamic nucleus, intermediodorsal nucleus, paracentral nucleus, interanteromedial nucleus, reuniens nucleus), hypothalamus (acruate nucleus, medial tubereal nucleus, infundibular stalk), midbrain and pons (ventral tegmental area, interpeduncular nucleus rostral apical and caudal subnucleus, dorsal raphe nucleus, rostral linear nucleus of the raphe, median raphe nucleus, dorsal nucleus of the lateral lemniscus, pedunculopontine tegmental nucleus, pontine reticular nucleus oral part, pontine nuclei, reticulotegmental nucleus of the pons, dorsal tegmental nucleus, laterodorsal tegmental nucleus, venral tegemental nucleus), pontine reticular nucleus caudal part, superior periolivary nucleus, lateral and medial superior olivary nucleus), Medulla (parvocellular reticular nucleus, intermediate reticular nucleus, gigantocellular reticular nucleus, paragigantocellular nucleus, raphe magnus nucleus, raphe pallidus nucleus, rostroventricular reticular nucleus, medullary reticular nucleus ventral part, medullary reticular nucleus dorsal part, lateral reticular nucleus, praepositus hypoglossal nucleus, inferior olivary complex principal and dorsal nuclei, gracilis nucleus, cuneate nucleus, area postrema), cranial nerve nucei (cochlear nuclei dorsal nucleus, cochlear nuclei vestibular nuclei superior, medial, lateral and spinal nuclei), cerebellum (granule cell layer Golgi type II cells)
Expression level:  Medium
Species:  Rat
Technique:  Immunohistochemistry.
References:  12,36
Thalamic nuclei and basal ganglia. In all thalamic nuclei this subunit is expressed at a moderate level. At centrolateral nucleus, parafascicular and paracentral nuclei the expression level is high. In substantia nigra compacta the expression of α3 subunits was high, in all other basal ganglia nuclei it is moderate
Species:  Rhesus macaque
Technique:  In situ hybridisation
References:  20,26
Physiological Consequences of Altering Gene Expression
Electrophysiolgical phenotype

In midbrain dopaminergic neurons of α3 KO mice, whole-cell GABA-induced currents are decreased, consistent with the α3 subunit being the major α subunit in these neurons (Yee et al., 2005).
Species:  Mouse
Tissue: 
Technique:  Gene knockout
References:  50
The regional distribution of α1, α2, and α5 subunits is unaltered in mice with a global knockout of the α3 subunit (α3 KO mice) (Yee et al., 2005; Studer et al., 2006). Whereas in wild type mice the α3 and α2 subunits are clustered at postsynaptic sites in the thalamic reticular nucleus along with gephyrin, in the α3 KO mice γ2 clustering was disrupted and gephyrin formed large aggregates localized at the cell surface (Studer et al., 2006), indicating that the α3 KO mice lack postsynaptic GABAA receptors in the reticular nucleus (Studer et al., 2006). In the α3 KO mice, GABAergic terminals were enlareged and reduced in number, suggesting a partial deficit of GABAergic synapses (Studer et al., 2006).

Behavioral phenotypes

Mice with a knockout of the α3 subunit (α3 KO mice) display an increased locomotor activity in a novel open field and on the elevated plus maze (Yee et al., 2005). In the elevated plus maze test, a test of unconditioned anxiety, the % time α3 KO mice spent in the open arms was indistinguishable from wild type (Yee et al., 2005). Diazpeam increases the % time spent in the open arms. These findings indicate that anxiety-like behavior is not changed in these animals (Yee et al., 2005). α3 KO exhibit a deficit in prepulse inhibition (PPI) to acoustic startle, indicating a deficit in sensorimotor gating; this deficit can be corrected with the D2-antagonist haloperidol (Yee et al., 2005). The PPI findings, the increased locomotor activity, an the presence of the α3 subunit in dopaminergic neurons are consistent with an increased activity of midbrain dopaminergic neurons in the α3 KO mice. In the forced swim test, a test of behavioral despair, α3 KO mice exhibited reduced floating and enhanced swimming behavior, potentially indicating an antidepressant-like phenotype (Fiorelli et al., 2008). Sucrose preference was unaltered (Fiorelli et al., 2008). In the one-bottle forced sucrose consumption test across different sucrose concentrations, an enhanced negative contrast was observed: when the sucrose concentration was reduced from 1% to 0.5%, α3 KO mice showed a decrease in consumption, in contrast to wild type mice (Fiorelli et al., 2008). In Pavlovian fear conditioning, wild type mice reacted significantly stronger to the tone than to the context; this difference was reduced in α3 KO mice (Fiorelli et al., 2008). Performance in the Morris water maze task was indistinguishable from wild type (Fiorelli et al., 2008).

α3 KO mice display normal sleep homeostasis and no changes in the EEG suggestive of absence seizures, potentially pointing to compensations of the knockout (Winsky-Sommerer et al., 2008). Indeed, the inhibitory postsynaptic response in the reticular nucleus of the thalamus displays a powerful compensatory gain, so that evoked thalamic oscillations and pharmacologically induced absence seizures showed a reduction in length and power (Schofield et al., 2009). 
Species:  Mouse
Tissue: 
Technique:  Gene knockout
References:  11,40,46-47,50
Mice have been generated which have a histidine to arginine point mutation at position 126 in the α3 subunit, which abolished binding of diazepam (Low et al., 2000).

Behavioral phenotypes

The anxiolytic, sedative, and anticonvulsant actions of diazepam were intact in the α3(H126R) mice, indicating that α3-containing GABAA receptors are not required for these actions (Low et al., 2000). The muscle relaxant action of diazepam was reduced, suggesting that α3-containing GABAA receptors contribute to this effect (Crestani et al., 2001).

The analgesia induced by intrathecally administered diazepam is reduced in α3(126R) in models of inflammatory and neuropathic pain, indicating that α3-containing GABAA receptors contribute to the analgesic actions of diazepam; this effect is attributed to spinal α3-containing GABAA receptors (Knabl et al., 2008). In the formalin test, a model of tonic nociception, systemically administered diazepam had a reduced effect in α1(H101R)/ α3(H126R) double mutant mice, indicating a role for α3-containing GABAA receptors in tonic nociception (Knabl et al., 2009).

Diazepam-induced changes on sleep and the EEG spectrum in α3(H126R) mice were indistinguishable from wild type mice, indicating that α3-containing GABAA receptors are not required for these changes (Kopp et al., 2003).

Electrophysiological phenotypes

Studies in α3(H126R) established that the suppression of thalamic oscillations by clonazepam results exclusively from its action on α3-containing GABAA receptors in the thalamic reticular nucleus (Sohal et al., 2003).
Species:  Mouse
Tissue: 
Technique:  α3(H126R) knock-in point mutation
References:  8,23-25,30,44
In the Wistar albino Glaxo/Rij (WAG-Rij) rat, which is recognized as a genetic model for absence epilepsy, a specific loss of α3 immunoreactivity was detected in inhibitory synapses in the reticular nucleus of the thalamus, while the α3 mRNA levels were unaltered, suggesting a role of these α3-containing GABAA receptors in the phenotype of this rat model (Liu et al., 2007)
Species:  Rat
Tissue: 
Technique:  Rat inbred strain
References:  27
In human genetic studies, the gene encoding the α3 subunit has been linked to unipolar depressive disorder (Henkel et al., 2004), bipolar disorder (Massat et al., 2002), neuroleptic-induced, treatment-resistant tardive dyskinesia (Inada et al., 2008), and multiple sclerosis (Gade-Andavolu et al., 1998). The association with multiple sclerosis was suggested to be due to its regulation of prolactin release (Gade-Andavolu et al., 1998). However, the associations with with unipolar depression and bipolar depression could not be confirmed in other studies (Bosker et al., 2010; Craddock et al., 2010; Puertollano et al., 1995). An association has also been found with thyrotoxic hypokalaemic periodic paralysis (Jongjaroenprasert et al., 2008). The α3 subunit is downregulated in autism (Fatemi et al., 2009).
Species:  Human
Tissue: 
Technique: 
References:  4,7,10,13,16,21-22,31,38
Clinically-Relevant Mutations and Pathophysiology
Disease:  Thyrotoxic periodic paralysis
Orphanet: ORPHA79102
References:  22
Gene Expression and Pathophysiology
Overexpression
Tissue or cell type:  HCC (hepatocellular carcionoma) cell line Chang, HepG2, 6/8 HCC tissue samples
Pathophysiology:  α3 subunit expression appears to correlate with growth in the presence of GABA.
Species:  Human
Technique: 
References:  29
Overexpression
Tissue or cell type:  Lung cancer, endometrial cancer, glioma
Pathophysiology:  The α3 subunit is overexpressed in lung cancer, and was found in 12/12 lung cancer tissue samples and only a few other cancers and may thus be useful as a biomarker. Expression of α3 was significantly higher in lower grade lung cancer. α3 was also expressed in 11/11 endometrial cancer tissue samples, and 3/3 glioma tissue samples.
Species:  Human
Technique: 
References:  28
Biologically Significant Variants
Type:  Pre-mRNA editing
Species:  Mouse
Description:  Gabra3 pre-mRNA undergoes A- to-I editing. See section "General comment on the subunit".
General Comments
The α3 subunit pre-mRNA is subject to A- to -I editing by the enzymes ADAR(adenosine desaminase that acts on RNA)1 and ADAR2; this editing recodes an isoleucine in the third transmembrane region to a methionine (which is also referred to as I/M site [33]. Editing is low at embryonic day 15, and reaches maximal levels on postnatal day 7 [39]. In adult mice, approximately 90%-95% of the Gabra3 transcripts are edited in most regions of the brain, only in the hippocampus editing is lower (70%) [39]. Receptors containing the non-edited α3 subunit are activated more rapidly and deactivated more slowly than receptor containing the edited α3 subunit [32,39]. Moreover, currents from non-edited receptors are strongly outward rectifying (corresponding to chloride influx), whereas edited receptors have a more linear current/voltage relationship [39]. It has been suggested that the non-edited version of the α3 subunit which is expressed early in development when GABA is depolarizing may allow the robust excitatory responses that are critical for synapse formation, and it could also help to prevent excessive excitation [39]. Editing has also been shown to reduced the cell surface and the total number of α3 subunits in a recombinant system in HEK293 cells, suggesting that editing plays a role in receptor trafficking [9].

References

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4. Bosker FJ, Hartman CA, Nolte IM, Prins BP, Terpstra P, Posthuma D, van Veen T, Willemsen G, DeRijk RH, de Geus EJ et al.. (2011) Poor replication of candidate genes for major depressive disorder using genome-wide association data. Mol. Psychiatry16 (5): 516-32. [PMID:20351714]

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7. Craddock N, Jones L, Jones IR, Kirov G, Green EK, Grozeva D, Moskvina V, Nikolov I, Hamshere ML, Vukcevic D et al.. (2010) Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype. Mol. Psychiatry15 (2): 146-53. [PMID:19078961]

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9. Daniel C, Wahlstedt H, Ohlson J, Björk P, Ohman M. (2011) Adenosine-to-inosine RNA editing affects trafficking of the gamma-aminobutyric acid type A (GABA(A)) receptor. J. Biol. Chem.286 (3): 2031-40. [PMID:21030585]

10. Fatemi SH, Reutiman TJ, Folsom TD, Thuras PD. (2009) GABA(A) receptor downregulation in brains of subjects with autism. J Autism Dev Disord39 (2): 223-30. [PMID:18821008]

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13. Gade-Andavolu R, MacMurray JP, Blake H, Muhleman D, Tourtellotte W, Comings DE. (1998) Association between the gamma-aminobutyric acid A3 receptor gene and multiple sclerosis. Arch. Neurol.55 (4): 513-6. [PMID:9561979]

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15. Hadingham KL, Wingrove P, Le Bourdelles B, Palmer KJ, Ragan CI, Whiting PJ. (1993) Cloning of cDNA sequences encoding human alpha 2 and alpha 3 gamma-aminobutyric acidA receptor subunits and characterization of the benzodiazepine pharmacology of recombinant alpha 1-, alpha 2-, alpha 3-, and alpha 5-containing human gamma-aminobutyric acidA receptors. Mol. Pharmacol.43 (6): 970-5. [PMID:8391122]

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Uwe Rudolph, Werner Sieghart.
GABAA receptors: GABAA receptor α3 subunit. Last modified on 04/04/2016. Accessed on 21/07/2017. IUPHAR/BPS Guide to PHARMACOLOGY, http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=406.