GABA is the main inhibitory neurotransmitter in the postnatal animal brain: it is supposed to account for 30% of central synapses, where it binds to ionotropic (GABAARs) and metabotropic (GABABRs) receptors. As anion channels, GABAARs mediate fast inhibitory transmission, and they have been associated to a variety of physiological functions and dysfunctions in the brain, including sedation, anxiolysis, cognitive impairments, myorelaxation, pain management, addiction, or autism. They are targeted by genetic mutations which can generate channelopathies, and a variety of molecules from natural or synthetic origins. Moreover, many non-neuronal cells also express GABAARs.
The recent experimental elucidation of the 3D structure of GABAARs opens unprecedented perspectives to understand their interactions with such molecules. In fact, there is a large number of chemicals that target this channel at different binding sites, and play an agonist, antagonist or allosteric modulator role. In therapeutics, benzodiazepines are the most commonly used drugs for anxiety management. Different classes of insecticides block the chloride channel of GABAARs, with deleterious consequences on the mammalian brain. Animal or plant toxins have been shown to facilitate or reduce GABAergic transmission with an adaptive benefit. The GABAAR subunit composition appears as a crucial feature to understand their pharmacological properties and the physiological consequences. In addition, recent identification of GABAAR auxiliary subunits adds a new dimension to understanding the regulation of receptor pharmacology.
This Research Topic is open to scientists with a broad interest on GABAARs in a mechanistic approach, at different scales (in silico, in vitro, in vivo). We wish to gather recent advances on GABAARs from all disciplines (pharmacology, biochemistry, behavioral, electrophysiology, genetic etc.) to highlight the functioning of GABAARs and their implication in the nervous system and in non-neuronal tissues. Original research articles, review articles and short communications are welcome.
GABA is the main inhibitory neurotransmitter in the postnatal animal brain: it is supposed to account for 30% of central synapses, where it binds to ionotropic (GABAARs) and metabotropic (GABABRs) receptors. As anion channels, GABAARs mediate fast inhibitory transmission, and they have been associated to a variety of physiological functions and dysfunctions in the brain, including sedation, anxiolysis, cognitive impairments, myorelaxation, pain management, addiction, or autism. They are targeted by genetic mutations which can generate channelopathies, and a variety of molecules from natural or synthetic origins. Moreover, many non-neuronal cells also express GABAARs.
The recent experimental elucidation of the 3D structure of GABAARs opens unprecedented perspectives to understand their interactions with such molecules. In fact, there is a large number of chemicals that target this channel at different binding sites, and play an agonist, antagonist or allosteric modulator role. In therapeutics, benzodiazepines are the most commonly used drugs for anxiety management. Different classes of insecticides block the chloride channel of GABAARs, with deleterious consequences on the mammalian brain. Animal or plant toxins have been shown to facilitate or reduce GABAergic transmission with an adaptive benefit. The GABAAR subunit composition appears as a crucial feature to understand their pharmacological properties and the physiological consequences. In addition, recent identification of GABAAR auxiliary subunits adds a new dimension to understanding the regulation of receptor pharmacology.
This Research Topic is open to scientists with a broad interest on GABAARs in a mechanistic approach, at different scales (in silico, in vitro, in vivo). We wish to gather recent advances on GABAARs from all disciplines (pharmacology, biochemistry, behavioral, electrophysiology, genetic etc.) to highlight the functioning of GABAARs and their implication in the nervous system and in non-neuronal tissues. Original research articles, review articles and short communications are welcome.
