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Relevant bibliographies by topics / GABAOA

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Journal articles

Academic literature on the topic 'GABAOA'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "GABAOA"

1

Park, Anthony, Kathleen Hoffman, and Asaf Keller. "Roles of GABAA and GABAB receptors in regulating thalamic activity by the zona incerta: a computational study." Journal of Neurophysiology 112, no. 10 (2014): 2580–96. http://dx.doi.org/10.1152/jn.00282.2014.

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The posterior thalamic nucleus (PO) is a higher order nucleus heavily implicated in the processing of somatosensory information. We have previously shown in rodent models that activity in PO is tightly regulated by inhibitory inputs from a GABAergic nucleus known as the zona incerta (ZI). The level of incertal inhibition varies under both physiological and pathological conditions, leading to concomitant changes in PO activity. These changes are causally linked to variety of phenomena from altered sensory perception to pathological pain. ZI regulation of PO is mediated by GABAA and GABAB recept

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2

Lu, Yong, R. Michael Burger, and Edwin W. Rubel. "GABAB Receptor Activation Modulates GABAA Receptor-Mediated Inhibition in Chicken Nucleus Magnocellularis Neurons." Journal of Neurophysiology 93, no. 3 (2005): 1429–38. http://dx.doi.org/10.1152/jn.00786.2004.

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Neurons of nucleus magnocellularis (NM), a division of avian cochlear nucleus that performs precise temporal encoding, receive glutamatergic excitatory input solely from the eighth nerve and GABAergic inhibitory input primarily from the ipsilateral superior olivary nucleus. GABA activates both ligand-gated Cl− channels [GABAA receptors (GABAARs)] and G protein-coupled receptors (GABAB receptors). The net effect of GABAAR-mediated input to NM is inhibitory, although depolarizing. Several studies have shown that this shunting, inhibitory GABAergic input can evoke action potentials in postsynapti

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3

Jones, S. M., and M. J. Palmer. "Activation of the Tonic GABAC Receptor Current in Retinal Bipolar Cell Terminals by Nonvesicular GABA Release." Journal of Neurophysiology 102, no. 2 (2009): 691–99. http://dx.doi.org/10.1152/jn.00285.2009.

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Within the second synaptic layer of the retina, bipolar cell (BC) output to ganglion cells is regulated by inhibitory input to BC axon terminals. GABAA receptors (GABAARs) mediate rapid synaptic currents in BC terminals, whereas GABAC receptors (GABACRs) mediate slow evoked currents and a tonic current, which is strongly regulated by GAT-1 GABA transporters. We have used voltage-clamp recordings from BC terminals in goldfish retinal slices to determine the source of GABA for activation of these currents. Inhibition of vesicular release with concanamycin A or tetanus toxin significantly inhibit

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4

Cifelli, Pierangelo, Silvia Di Angelantonio, Veronica Alfano, et al. "Dissecting the Molecular Determinants of GABAA Receptors Current Rundown, a Hallmark of Refractory Human Epilepsy." Brain Sciences 11, no. 4 (2021): 441. http://dx.doi.org/10.3390/brainsci11040441.

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GABAA receptors-(Rs) are fundamental for the maintenance of an efficient inhibitory function in the central nervous system (CNS). Their dysfunction is associated with a wide range of CNS disorders, many of which characterized by seizures and epilepsy. Recently, an increased use-dependent desensitization due to a repetitive GABA stimulation (GABAA current rundown) of GABAARs has been associated with drug-resistant temporal lobe epilepsy (TLE). Here, we aimed to investigate the molecular determinants of GABAA current rundown with two different heterologous expression systems (Xenopus oocytes and

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5

Ando, Yuko, Minoru Hojo, Masato Kanaide та ін. "S (+)-Ketamine Suppresses Desensitization of γ-Aminobutyric Acid Type B Receptor-mediated Signaling by Inhibition of the Interaction of γ-Aminobutyric Acid Type B Receptors with G Protein–coupled Receptor Kinase 4 or 5". Anesthesiology 114, № 2 (2011): 401–11. http://dx.doi.org/10.1097/aln.0b013e318204e003.

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Background Intrathecal baclofen therapy is an established treatment for severe spasticity. However, long-term management occasionally results in the development of tolerance. One of the mechanisms of tolerance is desensitization of γ-aminobutyric acid type B receptor (GABABR) because of the complex formation of the GABAB2 subunit (GB2R) and G protein-coupled receptor kinase (GRK) 4 or 5. The current study focused on S(+)-ketamine, which reduces the development of morphine tolerance. This study was designed to investigate whether S(+)-ketamine affects the GABABR desensitization processes by bac

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6

Phillips, William D., and Stanley C. Froehner. "GABARAP and GABAA Receptor Clustering." Neuron 33, no. 1 (2002): 4–6. http://dx.doi.org/10.1016/s0896-6273(01)00569-4.

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7

Binet, V., C. Goudet, C. Brajon, et al. "Molecular mechanisms of GABAB receptor activation: new insights from the mechanism of action of CGP7930, a positive allosteric modulator." Biochemical Society Transactions 32, no. 5 (2004): 871–72. http://dx.doi.org/10.1042/bst0320871.

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The GABAB (γ-aminobutyric acid-B) receptor is composed of two subunits, GABAB1 and GABAB2. Both subunits share structural homology with other class-III G-protein-coupled receptors. They contain two main domains, a heptahelical domain typical of all G-protein-coupled receptors and a large ECD (extracellular domain). It has not been demonstrated whether the association of these two subunits is always required for function. However, GABAB2 plays a major role in coupling with G-proteins, and GABAB1 has been shown to bind GABA. To date, only ligands interacting with GABAB1-ECD have been identified.

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8

Muñoz, Mª, Nerea de la Fuente та Amelia Sánchez-Capelo. "TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson’s Disease". International Journal of Molecular Sciences 21, № 2 (2020): 590. http://dx.doi.org/10.3390/ijms21020590.

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γ-Aminobutiryc acid (GABA) is found extensively in different brain nuclei, including parts involved in Parkinson’s disease (PD), such as the basal ganglia and hippocampus. In PD and in different models of the disorder, an increase in GABA neurotransmission is observed and may promote bradykinesia or L-Dopa-induced side-effects. In addition, proteins involved in GABAA receptor (GABAAR) trafficking, such as GABARAP, Trak1 or PAELR, may participate in the aetiology of the disease. TGF-β/Smad3 signalling has been associated with several pathological features of PD, such as dopaminergic neurodegene

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9

Jung, Carole, Victor Fernández-Dueñas, Cristina Plata, et al. "Functional coupling of GABAA/B receptors and the channel TRPV4 mediates rapid progesterone signaling in the oviduct." Science Signaling 11, no. 543 (2018): eaam6558. http://dx.doi.org/10.1126/scisignal.aam6558.

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The molecular mechanism by which progesterone (P4) modulates the transport of ova and embryos along the oviduct is not fully resolved. We report a rapid response to P4 and agonists of γ-aminobutyric acid receptors A and B (GABAA/B) in the mouse oviduct that was characterized by oscillatory Ca2+ signals and increased ciliary beat frequency (CBF). Pharmacological manipulation, genetic ablation, and siRNA-mediated knockdown in oviductal cells, as well as overexpression experiments in HEK 293T cells, confirmed the participation of the cationic channel TRPV4, different subunits of GABAA (α1 to α3,

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10

Evenseth, Linn Samira Mari, Mari Gabrielsen, and Ingebrigt Sylte. "The GABAB Receptor—Structure, Ligand Binding and Drug Development." Molecules 25, no. 13 (2020): 3093. http://dx.doi.org/10.3390/molecules25133093.

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The γ-aminobutyric acid (GABA) type B receptor (GABAB-R) belongs to class C of the G-protein coupled receptors (GPCRs). Together with the GABAA receptor, the receptor mediates the neurotransmission of GABA, the main inhibitory neurotransmitter in the central nervous system (CNS). In recent decades, the receptor has been extensively studied with the intention being to understand pathophysiological roles, structural mechanisms and develop drugs. The dysfunction of the receptor is linked to a broad variety of disorders, including anxiety, depression, alcohol addiction, memory and cancer. Despite

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