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  • Presynaptic GABA(B) receptors decrease neurotransmitter release in vestibular nuclei neurons during vestibular compensation. 22871524

    Unilateral damage to the peripheral vestibular receptors precipitates a debilitating syndrome of oculomotor and balance deficits at rest, which extensively normalize during the first week after the lesion due to vestibular compensation. In vivo studies suggest that GABA(B) receptor activation facilitates recovery. However, the presynaptic or postsynaptic sites of action of GABA(B) receptors in vestibular nuclei neurons after lesions have not been determined. Accordingly, here presynaptic and postsynaptic GABA(B) receptor activity in principal cells of the tangential nucleus, a major avian vestibular nucleus, was investigated using patch-clamp recordings correlated with immunolabeling and confocal imaging of the GABA(B) receptor subunit-2 (GABA(B)R2) in controls and operated chickens shortly after unilateral vestibular ganglionectomy (UVG). Baclofen, a GABA(B) agonist, generated no postsynaptic currents in principal cells in controls, which correlated with weak GABA(B)R2 immunolabeling on principal cell surfaces. However, baclofen decreased miniature excitatory postsynaptic current (mEPSC) and GABAergic miniature inhibitory postsynaptic current (mIPSC) events in principal cells in controls, compensating and uncompensated chickens three days after UVG, indicating the presence of functional GABA(B) receptors on presynaptic terminals. Baclofen decreased GABAergic mIPSC frequency to the greatest extent in principal cells on the intact side of compensating chickens, with concurrent increases in GABA(B)R2 pixel brightness and percentage overlap in synaptotagmin 2-labeled terminals. In uncompensated chickens, baclofen decreased mEPSC frequency to the greatest extent in principal cells on the intact side, with concurrent increases in GABA(B)R2 pixel brightness and percentage overlap in synaptotagmin 1-labeled terminals. Altogether, these results revealed changes in presynaptic GABA(B) receptor function and expression which differed in compensating and uncompensated chickens shortly after UVG. This work supports an important role for GABA(B) autoreceptor-mediated inhibition in vestibular nuclei neurons on the intact side during early stages of vestibular compensation, and a role for GABA(B) heteroreceptor-mediated inhibition of glutamatergic terminals on the intact side in the failure to recover function.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • GABA(B) receptors do not internalize after baclofen treatment, possibly due to a lack of β-arrestin association: study with a real-time visualizing assay. 22517292

    The mechanism of agonist-induced GABA(B) receptor (GABA(B) R) internalization is not well understood. To investigate this process, we focused on the interaction of GABA(B) R with β-arrestins, which are key proteins in the internalization of most of the G protein-coupled receptors, and the agonist-induced GABA(B) R internalization and the interaction of GABA(B) R with β-arrestin1 and β-arrestin2 were investigated in real time using GABA(B) R and β-arrestins both of which were fluorescent protein-tagged. We then compared these profiles with those of μ-opioid receptors (μOR), well-studied receptors that associate and cointernalize with β-arrestins. When stimulated by the specific GABA(B) R agonist baclofen, GABA(B) R composed of GABA(B1a) R (GB(1a) R) and fluorescent protein-tagged GABA(B2) R-Venus (GB₂ R-V) formed functional GABA(B) R; they elicited G protein-activated inwardly rectifying potassium channels as well as nontagged GABA(B) R. In cells coexpressing GB(1a) R, GB₂ R-V, and β-arrestin1-Cerulean (βarr1-C) or β-arrestin2-Cerulean (βarr2-C), real-time imaging studies showed that baclofen treatment neither internalized GB₂ R-V nor mobilized βarr1-C or βarr2-C to the cell surface. This happened regardless of the presence of G protein-coupled receptor kinase 4 (GRK4), which forms a complex with GABA(B) R and causes GABA(B) R desensitization. On the other hand, in cells coexpressing μOR-Venus, GRK2, and βarr1-C or βarr2-C, the μOR molecule formed μOR/βarr1 or μOR/βarr2 complexes on the cell surface, which were then internalized into the cytoplasm in a time-dependent manner. Fluorescence resonance energy transfer assay also indicated scarce association of GB₂ R-V and β-arrestins-C with or without the stimulation of baclofen, while robust association of μOR-V with β-arrestins-C was detected after μOR activation. These findings suggest that GABA(B) Rs failure to undergo agonist-induced internalization results in part from its failure to interact with β-arrestins.
    Document Type:
    Reference
    Product Catalog Number:
    AP180
    Product Catalog Name:
    Donkey Anti-Goat IgG Antibody, Species Adsorbed - (Donkey Anti-Goat IgG Antibody, Species Adsorbed)

  • GABA B RECEPTOR R1 CONTROL PEPTIDE

    Document Type:
    Certificate of Analysis
    Lot Number:
    2899912
    Product Catalog Number:
    AG324
    Product Catalog Name:
    GABA B Receptor R1, control peptide for AB1531 - (GABA B Receptor R1, control peptide for AB1531)

  • GABA B RECEPTOR R1 CONTROL PEPTIDE - 2389530

    Document Type:
    Certificate of Analysis
    Lot Number:
    2389530
    Product Catalog Number:
    AG324
    Product Catalog Name:
    GABA B Receptor R1, control peptide for AB1531 - (GABA B Receptor R1, control peptide for AB1531)

  • GABA(B) receptor activation triggers BDNF release and promotes the maturation of GABAergic synapses. 19759312

    GABA, the main inhibitory neurotransmitter in the adult brain, has recently emerged as an important signal in network development. Most of the trophic functions of GABA have been attributed to depolarization of the embryonic and neonatal neurons via the activation of ionotropic GABA(A) receptors. Here we demonstrate a novel mechanism by which endogenous GABA selectively regulates the development of GABAergic synapses in the developing brain. Using whole-cell patch-clamp recordings on newborn mouse hippocampi lacking functional GABA(B) receptors (GABA(B)-Rs) and time-lapse fluorescence imaging on cultured hippocampal neurons expressing GFP-tagged brain-derived neurotrophic factor (BDNF), we found that activation of metabotropic GABA(B) receptors (GABA(B)-Rs) triggers secretion of BDNF and promotes the development of perisomatic GABAergic synapses in the newborn mouse hippocampus. Because activation of GABA(B)-Rs occurs during the characteristic ongoing physiological network-driven synaptic activity present in the developing hippocampus, our results reveal a new mechanism by which synaptic activity can modulate the development of local GABAergic synaptic connections in the developing brain.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • GABA B RECEPTOR R1 CONTROL PEPTIDE - 3577425

    Document Type:
    Certificate of Analysis
    Lot Number:
    3577425
    Product Catalog Number:
    AG324
    Product Catalog Name:
    GABA B Receptor R1, control peptide for AB1531 - (GABA B Receptor R1, control peptide for AB1531)

  • Mechanism of GABA(B) receptor-induced BDNF secretion and promotion of GABA(A) receptor membrane expression. 21255015

    J. Neurochem. (2011) 118, 533-545. ABSTRACT: Recent studies have shown that GABA(B) receptors play more than a classical inhibitory role and can function as an important synaptic maturation signal early in life. In a previous study, we reported that GABA(B) receptor activation triggers secretion of brain-derived neurotrophic factor (BDNF) and promotes the functional maturation of GABAergic synapses in the developing rat hippocampus. To identify the signalling pathway linking GABA(B) receptor activation to BDNF secretion in these cells, we have now used the phosphorylated form of the cAMP response element-binding protein as a biological sensor for endogenous BDNF release. In the present study, we show that GABA(B) receptor-induced secretion of BDNF relies on the activation of phospholipase C, followed by the formation of diacylglycerol, activation of protein kinase C, and the opening of L-type voltage-dependent Ca(2+) channels. We further show that once released by GABA(B) receptor activation, BDNF increases the membrane expression of β(2/3) -containing GABA(A) receptors in neuronal cultures. These results reveal a novel function of GABA(B) receptors in regulating the expression of GABA(A) receptor through BDNF-tropomyosin-related kinase B receptor dependent signalling pathway.
    Document Type:
    Reference
    Product Catalog Number:
    MAB341
    Product Catalog Name:
    Anti-GABA A Receptor β 2,3 Chain Antibody, clone BD17 - (Anti-GABA A Receptor β 2,3 Chain Antibody, clone BD17)

  • Antibodies to the GABA(B) receptor in limbic encephalitis with seizures: case series and characterisation of the antigen. 19962348

    Some encephalitides or seizure disorders once thought idiopathic now seem to be immune mediated. We aimed to describe the clinical features of one such disorder and to identify the autoantigen involved.15 patients who were suspected to have paraneoplastic or immune-mediated limbic encephalitis were clinically assessed. Confocal microscopy, immunoprecipitation, and mass spectrometry were used to characterise the autoantigen. An assay of HEK293 cells transfected with rodent GABA(B1) or GABA(B2) receptor subunits was used as a serological test. 91 patients with encephalitis suspected to be paraneoplastic or immune mediated and 13 individuals with syndromes associated with antibodies to glutamic acid decarboxylase 65 were used as controls.All patients presented with early or prominent seizures; other symptoms, MRI, and electroencephalography findings were consistent with predominant limbic dysfunction. All patients had antibodies (mainly IgG1) against a neuronal cell-surface antigen; in three patients antibodies were detected only in CSF. Immunoprecipitation and mass spectrometry showed that the antibodies recognise the B1 subunit of the GABA(B) receptor, an inhibitory receptor that has been associated with seizures and memory dysfunction when disrupted. Confocal microscopy showed colocalisation of the antibody with GABA(B) receptors. Seven of 15 patients had tumours, five of which were small-cell lung cancer, and seven patients had non-neuronal autoantibodies. Although nine of ten patients who received immunotherapy and cancer treatment (when a tumour was found) showed neurological improvement, none of the four patients who were not similarly treated improved (p=0.005). Low levels of GABA(B1) receptor antibodies were identified in two of 104 controls (pless than 0.0001).GABA(B) receptor autoimmune encephalitis is a potentially treatable disorder characterised by seizures and, in some patients, associated with small-cell lung cancer and with other autoantibodies.National Institutes of Health.
    Document Type:
    Reference
    Product Catalog Number:
    AB2256
    Product Catalog Name:
    Anti-GABA B Receptor R1 Antibody - (Anti-GABA B Receptor R1 Antibody)

  • Differential expression of GABA(B)R1 and GABA(B)R2 receptor immunoreactivity in neurochemically identified neurons of the rat neostriatum. 11304711

    Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the neostriatum. Functions of GABA are known to mediate GABA(A) and GABA(B) receptors. A functional GABA(B) receptor is known to compose of heteromeric subunits, namely the GABA(B)R1 and GABA(B)R2 subunits. Our previous report (Yung et al. [1999] Brain Res. 830:345-352) has demonstrated that all major subpopulations of striatal neurons express GABA(B)R1 immunoreactivity. The cellular localization of the second subunit of GABA(B) receptor protein, i.e., GABA(B)R2 immunoreactivity, in the rat neostriatum is not yet known. By using a new commercially available specific antibody against GABA(B)R2, immunofluorescence was performed to investigate the cellular expression of GABA(B)R2 in neurochemically identified subpopulations of neurons in the rat neostriatum. Immunoreactivity for GABA(B)R2 was primarily found in the neuropil of the rat neostriatum. Double labeling revealed that those perikarya that expressed immunoreactivity for parvalbumin, choline acetyltransferase, nitric oxide synthase, glutamate receptor two, N-methyl-D-aspartate receptor one, or GABA(A)alpha1 receptor, respectively, did not express GABA(B)R2 immunoreactivity. In addition, perikarya and most of the neuropilar elements in the neostriatum that expressed glutamic acid decarboxylase 67 immunoreactivity were found to be GABA(B)R2-negative. In contrast, immunoreactivity for GABA(B)R1 was found to be expressed by all of the above neuronal subpopulations. Moreover, a vast number of SV2-immunoreactive profiles and a number of tyrosine hydroxylase-immunoreactive profiles in the neuropil of the neostriatum were found to display GABA(B)R2 immunoreactivity. The present results indicate that there is a differential expression of GABA(B)R2 and GABA(B)R1 immunoreactivity in different subpopulations of striatal neurons that are identified by their specific neurochemical markers. Immunoreactivity for GABA(B)R2 is likely to localize in neuropilar elements of the neostriatum that may belong to non-GABAergic elements. These findings provide anatomical evidence of GABA(B)R2 receptor localization in the neostriatum that may have an important functional implication of the GABA(B)-mediated functions in neurons of the neostriatum.
    Document Type:
    Reference
    Product Catalog Number:
    AB1529
    Product Catalog Name:
    Anti-Nitric Oxide Synthase I Antibody - (Anti-Nitric Oxide Synthase I Antibody)

  • The level and distribution of the GABA(B)R1 and GABA(B)R2 receptor subunits in the rat's inferior colliculus. 23189044

    The type B γ-aminobutyric acid receptor (GABA(B) receptor) is an important neurotransmitter receptor in the midbrain auditory structure, the inferior colliculus (IC). A functional GABA(B) receptor is a heterodimer consisting of two subunits, GABA(B)R1 and GABA(B)R2. Western blotting and immunohistochemical experiments were conducted to examine the expression of the two subunits over the IC including its central nucleus, dorsal cortex, and external cortex (ICc, ICd, and ICx). Results revealed that the two subunits existed in both cell bodies and the neuropil throughout the IC. The two subunits had similar regional distributions over the IC. The combined level of cell body and neuropil labeling was higher in the ICd than the other two subdivisions. Labeling in the ICc and ICx was stronger in the dorsal than the ventral regions. In spite of regional differences, no defined boundaries were formed between different areas. For both subunits, the regional distribution of immunoreactivity in the neuropil was parallel to that of combined immunoreactivity in the neuropil and cell bodies. The density of labeled cell bodies tended to be higher but sizes of cell bodies tended to be smaller in the ICd than in the other subdivisions. No systematic regional changes were found in the level of cell body immunoreactivity, except that GABA(B)R2-immunoreactive cell bodies in the ICd had slightly higher optic density (OD) than in other regions. Elongated cell bodies existed throughout the IC. Many labeled cell bodies along the outline of the IC were oriented in parallel to the outline. No strong tendency of orientation was found in labeled cell bodies in ICc. Regional distributions of the subunits in ICc correlated well with inputs to this subdivision. Our finding regarding the contrast in the level of neuropil immunoreactivity among different subdivisions is consistent with the fact that the GABA(B) receptor has different pre- and postsynaptic functions in different IC regions.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple