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anti-Rat (Rattus) GABRA5 Antikörper:
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Mouse (Murine) Polyclonal GABRA5 Primary Antibody für WB - ABIN152536
Maison, Rosahl, Homanics, Liberman: Functional role of GABAergic innervation of the cochlea: phenotypic analysis of mice lacking GABA(A) receptor subunits alpha 1, alpha 2, alpha 5, alpha 6, beta 2, beta 3, or delta. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2006
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Chicken Polyclonal GABRA5 Primary Antibody für WB - ABIN550207
McKernan, Rosahl, Reynolds, Sur, Wafford, Atack, Farrar, Myers, Cook, Ferris, Garrett, Bristow, Marshall, Macaulay, Brown, Howell, Moore, Carling, Street, Castro, Ragan, Dawson, Whiting: Sedative but not anxiolytic properties of benzodiazepines are mediated by the GABA(A) receptor alpha1 subtype. in Nature neuroscience 2000
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GABRA5 receptor plays a unique role in reinforcing the effects of alcohol.
evaluated the role of alpha1 and alpha5 subunit-containing GABAA receptors (alpha1GABAA and alpha5GABAA receptors, respectively) in the ability of benzodiazepine-type drugs to alter performance in the cognitive domain of executive function
cryo-EM structure of the human alpha5beta3 GABAA receptor
The GABRA5 p.V294L variant produced receptors that were 10-times more sensitive to GABA but had reduced maximal GABA-evoked current due to increased receptor desensitization.
Meta-analysis showed that GABRA5 polymorphisms are not significantly associated with autism.
GABAA receptor gene polymorphisms can predict symptom-based and developmental deficits in autistic spectrum disorders individuals.
Low GABRA5 expression typified hyperproliferative tumors, and loss of taurine signaling correlated with reduced patient survival, suggesting this tumor suppressive mechanism operates in vivo.
Study found a significant reduction in [(11)C]Ro15 4513 binding in the nucleus accumbens in an opiate-dependent compared with the healthy control group. Study suggests that reduced GABA A receptor alpha5 levels in the nucleus accumbens are associated with addiction.
Report benzodiazepine derivative as GABA-site inhibitor of extra-synaptic GABAA alpha5 receptors.
Study found that a significant portion of GABAergic postsynaptic compartments contain the alpha5 GABAAR subunit, both in vitro and in vivo
This study showed that in male groups, the expression of GABRA5 was generally lower in schizophrenia cases compared to the control.
Findings provide genetic evidence for the involvement of the genes GABRB3 and GABRA5 in the susceptibility to panic disorder
1,2-dichlorohexafluorocyclobutane enhancement of GABRA5 activity is abolished by GABRB3 mutations.
The alpha5 nicotinic receptor GABAergic neurons form a link from the medial habenula to the serotonergic brain centers.
These results provide initial evidence of a GABAA alpha5 deficit in autism spectrum disorder and support further investigations of the GABA system in this disorder.
In subjects with schizophrenia, mean GABA (A) alpha5 rerceptor subunit mRNA expression is 15% lower in layer 4 of the dorsolateral prefrontal cortex.
Data indicate the selectivity of some selected compounds were assessed in recombinant alpha(1)beta(2)gamma(2)L, alpha(2)beta(1)gamma(2)L, and alpha(5)beta(2)gamma(2)L GABA(A) receptors.
The ratios of beta(3)/beta(2) and alpha(5)/alpha(1) subunit protein expression in Angelman syndrome cortex were significantly decreased when compared with controls.
extracellular domain models show subunit arrangement of GABA-A receptors
These results suggest that the GABRA5 gene may confer susceptibility to bipolar I disorder.
GABA(A) receptor alpha5 subunit as a candidate gene for autism and bipolar disorder; observations suggest parent-of-origin and gain-of-function effects
These results provide further evidence of the role of GABAA alpha5 receptor-mediated inhibition in cognitive impairment in the TS mouse model of Down syndrome.
Nonlinear-rectifying alpha5-GABAARs with slow kinetics match functional NMDA-receptor properties and thereby mediate powerful control of dendritic postsynaptic integration and action potential firing by dendrite-targeting interneurons.
findings support the hypothesis that reduced alpha5GABAAR activity contributes to an Autism Spectrum Disorder phenotype. The results also suggest that Gabra5-/- mice may serve as an animal model for ASD, as assessed through EEG activity and sleep-wake behaviors.
Deletion of Gabra5 in newborn granule cells caused severe alterations of migration and dendrite development.
In the present study explored the contribution of alpha5 subunit-containing GABAARs to tonic inhibition in the dorsal horn and pain processing.
Results suggest that alpha1, alpha5 and gamma2-containing hippocampal GABA type A receptors complexes play an essential role in spatial learning and memory in which targeted disruption of the alpha1 subunit produces profound deficits.
In conclusion, our findings reveal a role of alpha5-GABAARs in mediating the affective component of benzodiazepine-induced anxiolysis.
This study describes a novel mechanism that regulates plasma receptor pools in the control of synaptic receptor density.
This study demonstrated that alpha5-GABAAR-mediated tonic inhibition in the DG plays an important role in ensuring normal cognitive functioning under high-interference memory conditions.
Thus, alpha5GABA(A)R function does not return to baseline after the anesthetic is eliminated, suggesting a mechanism to account for persistent memory deficits after general anesthesia.
The results of this study suggested that gabra5 mediated tonic current, which is potentiated by H2O2, might contribute to H2O2-induced brain dysfunction.
in mice that lack the alpha5 subunit gene (Gabra5-/-), cultured embryonic hippocampal pyramidal neurons and ex vivo CA1 hippocampal neurons unexpectedly exhibited a decrease in Ih current density
alpha5GABA(A) receptor activity increases during inflammation and that this increase is critical for inflammation-induced memory deficits.
Gabra5-gene haplotype block associated with behavioral properties of the full agonist benzodiazepine chlordiazepoxide.
Data suggest that chronic exposure to ketamine impairs working memory in mice, which may be explained at least partly by up-regulation of Gabra5 subunits in the prefrontal cortex.
the results of this study suggested that the alpha5-subunit containing gamma-aminobutyric acid subtype A receptors are not direct targets for positive modulation by ethanol nor do they contribute to ethanol-induced memory loss.
Findings identify in alpha5(H105R) knockin mice a behavioral-cognitive phenotype affecting basal locomotion and the memory for location of objects indicative of hippocampal dysfunction resulting from moderately decreased alpha5-subunit contents.
under specific conditions, alpha5GABA(A)R activity predominates over synaptic inhibition in modifying the strength of both synaptic plasticity in vitro and certain forms of memory in vivo
These results show that alpha5GABA(A)R-mediated phasic inhibition is activated by the Schaffer collateral pathway and provide evidence for activity pattern-dependent participation of alpha5GABA(A)Rs in inhibition.
GABA is the major inhibitory neurotransmitter in the mammalian brain where it acts at GABA-A receptors, which are ligand-gated chloride channels. Chloride conductance of these channels can be modulated by agents such as benzodiazepines that bind to the GABA-A receptor. At least 16 distinct subunits of GABA-A receptors have been identified. Transcript variants utilizing three different alternative non-coding first exons have been described.
gamma-aminobutyric acid (GABA) A receptor, alpha 5
, gamma-aminobutyric acid A receptor, alpha 5-like
, gamma-aminobutyric acid receptor subunit alpha-5-like
, GABA(A) receptor subunit alpha-5
, GABA-A receptor alpha-5 subunit
, gamma-aminobutyric acid A receptor, alpha 5
, gamma-aminobutyric acid (GABA-A) receptor, subunit alpha 5
, gamma-aminobutyric acid A receptor, alpha 5
, gamma-aminobutyric acid receptor subunit alpha-5
, GABAA receptor alpha5 subunit
, ligand-gated ion channel subunit