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Tranquilizers/Anxiolytics: Pharmacology and Biochemistry of Anxiolytic Drugs Acting via GABAergic Mechanisms

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NeuroPsychopharmacotherapy

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Abstract

Both benzodiazepine tranquillizers and their predecessors, the barbiturates, achieve their effects by facilitating neurotransmission at inhibitory synapses employing the brain’s major inhibitory neurotransmitter, γ-aminobutyric acid (GABA), acting at the GABAA subtype of GABA receptor. Benzodiazepines differ from barbiturates in that they act only to facilitate the ability of the natural transmitter, GABA, to open channels in the neuronal membrane allowing chloride (and bicarbonate) ions to enter the neuron, normally causing hyperpolarization of the membrane, thereby reducing its response to excitatory events; in contrast, barbiturates, at sufficient concentrations, may directly open the chloride channels even in the absence of GABA release from presynaptic terminals. GABAA receptor complexes sensitive to benzodiazepines are made up of 5 proteins from 3 families, each existing in several isoforms, α1−5, β1−3, and γ1−3, whose distribution in the brain differ. Benzodiazepine-sensitive receptors are pentamers made up of 2α, 2β, and a single γ subunits, with α1, α2, α3, or α5 combining with β subunits, and γ2 subunit. Barbiturates are less selective and may act at additional receptor subtypes, including receptors located extrasynaptically. Animal research using mutated receptors has suggested that the anxiolytic effects of benzodiazepines are mediated by receptors employing the α2, and possibly the α3 subunit variant, while their sedative effects may be mediated by α1-containing complexes. While certain hypnotic drugs such as zolpidem may show some selectivity for receptors carrying the α1 subtype, drugs selective for either α2 or α3 receptors are not yet available. It is not clear whether the problems of abuse of, or dependence on benzodiazepine tranquillizers can be ascribed to actions at any particular subtypes of receptor. Despite being structurally related to GABA, more recently introduced Gabapentinoid tranquillizers appear to act via α2-δ calcium channel subunits. Other currently used anxiolytic drugs achieve their effects through actions at serotonin receptors.

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  1. School of Psychology, University of Sussex, Brighton, UK

    David N. Stephens

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  1. David N. Stephens
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  1. Clinic and Policlinic for Psychiatry, Psychosomatics and Psychotherapy, University Hospital Wuerzburg, Wuerzburg, Germany

    Peter Riederer

  2. Institute of Psychological Medicine (IPM), Soyen, Germany

    Gerd Laux

  3. Centre for Research Promotion and Support, Fujita Health University, Toyoake, Aichi, Japan

    Toshiharu Nagatsu

  4. Center Translational Res Neurol Diseases, Dalian Med Uni Shanghai Inst Health Sc Center Translational Res Neurol Diseases, Dalian, China

    Weidong Le

  5. Würzburg, Germany

    Christian Riederer

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  1. Centre for Addiction and Mental Health; Department of Psychiatry, University of Toronto, Toronto, ON, Canada

    Stefan Kloiber

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Stephens, D.N. (2022). Tranquilizers/Anxiolytics: Pharmacology and Biochemistry of Anxiolytic Drugs Acting via GABAergic Mechanisms. In: Riederer, P., Laux, G., Nagatsu, T., Le, W., Riederer, C. (eds) NeuroPsychopharmacotherapy. Springer, Cham. https://doi.org/10.1007/978-3-030-62059-2_61

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