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  2. GABA receptor agonist - Wikipedia

    en.wikipedia.org/wiki/GABA_receptor_agonist

    A GABA receptor agonist is a drug that is an agonist for one or more of the GABA receptors, producing typically sedative effects, and may also cause other effects such as anxiolytic, anticonvulsant, and muscle relaxant effects. [1]

  3. Sodium oxybate - Wikipedia

    en.wikipedia.org/wiki/Sodium_oxybate

    The full mechanism of action of sodium oxybate is poorly understood. [ 3 ] [ 7 ] GHB is a normal metabolite of GABA that interacts with the GABA B receptor and the GHB receptor . [ 3 ] It has been shown to enhance the restorativeness of sleep in part by altering sleep architecture in narcoleptic patients.

  4. Midazolam - Wikipedia

    en.wikipedia.org/wiki/Midazolam

    The therapeutic as well as adverse effects of midazolam are due to its effects on the GABA A receptors; midazolam does not activate GABA A receptors directly but, as with other benzodiazepines, it enhances the effect of the endogenous neurotransmitter GABA on the GABA A receptors (increasing the frequency of Cl − channel opening) resulting in ...

  5. GABA reuptake inhibitor - Wikipedia

    en.wikipedia.org/wiki/GABA_reuptake_inhibitor

    A GABA reuptake inhibitor (GRI) is a type of drug which acts as a reuptake inhibitor for the neurotransmitter gamma-Aminobutyric acid (GABA) by blocking the action of the gamma-Aminobutyric acid transporters (GATs). This in turn leads to increased extracellular concentrations of GABA and therefore an increase in GABAergic neurotransmission. [1]

  6. GABA - Wikipedia

    en.wikipedia.org/wiki/Piperidinate

    GABA is sold as a dietary supplement in many countries. It has been traditionally thought that exogenous GABA (i.e., taken as a supplement) does not cross the blood–brain barrier, but data obtained from more recent research (2010s) in rats describes the notion as being unclear. [2] [3] The carboxylate form of GABA is γ-aminobutyrate.

  7. Etifoxine - Wikipedia

    en.wikipedia.org/wiki/Etifoxine

    At GABA A receptors etifoxine binds at the α+β− interface and preferentially potentiates α 2 β 3 γ 2 and α 3 β 3 γ 2 receptor types. [25] This direct allosteric potentiation can only be observed at relatively high concentrations (starting at >1 mM) and is perhaps not physiologically relevant at normal human doses. [ 26 ]