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GABA receptors hypnotic drugs

Most hypnotic drugs act on GABA receptors. It is reasonable to hypothesize that hypnotic actions are mediated by the GABA receptors on wake-promoting neurons innervated by POA sleep-active neurons, but there is little study of this problem. However, there is evidence that GABAergic anesthetics induce c-Fos IR in the VLPO and suppress c-Fos IR in histaminergic neurons (Nelson et al, 2002). [Pg.17]

Sedation is an intermediate degree of CNS depression, while hypnosis is a degree of CNS depression similar to natural sleep. From the chemical point of view, soporific, sedative, and hypnotic drugs are classified as barbiturates, benzodiazepine hypnotics, and so on. Except for a few rare exceptions, any one of these compounds can be used for acquiring a sedative effect or state of sleep. Presently, the less toxic benzodiazepines are edging out the class of barbiturates more and more because of the possibility of chronic dependence associated with the use of barbiturates. Drugs of both classes are primarily CNS depressants, and a few of their effects, if not all, are evidently linked to action on the GABA-receptor complex. [Pg.57]

Another chemical class of sedative-hypnotic drugs, the barbiturates, also binds to receptors associated with the GABA-chloride ionophore, but these drugs appear to prolong rather than intensify GABA s effects. Fig. 24.4 shows the presumed drug receptor-GABA-chloride ionophore relationship. [Pg.357]

Aminobutyric acid (GABA) is the most important inhibitory neurotransmitter in the mammalian brain and localizes to approximately 30 % of central nervous system (CNS) synapses. This inhibitory neurotransmitter is of particular interest because most therapeutically useful hypnotic drugs work by selectively affecting GABA receptors. [Pg.211]

The sedative and hypnotic effects of benzo diazepines are accentuated by other drugs acting on the gamma-aminobutyric acid, (GABA ) receptor, especially barbiturates and alcohol. However, there are fewer drug... [Pg.206]

Pharmacology Zolpidem is a nonbenzodiazepine hypnotic. While zolpidem is a hypnotic agent with a chemical structure unrelated to benzodiazepines, barbiturates, or other drugs with known hypnotic properties, it interacts with a GABA-BZ receptor complex and shares some of the pharmacological properties of the benzodiazepines. [Pg.1179]

In contrast to GABA itself, benzodiazepines and other sedative-hypnotics have a low affinity for GABAB receptors, which are activated by the spasmolytic drug baclofen (see Chapters 21 and 27). [Pg.477]

The fundamental neurobiological importance of the GABA A receptor is underscored by observations that even more receptor sites exist at or near this complex (Fig. 8—20). This includes receptor sites for nonbenzodiazepine sedative-hypnotics such as zolpidem and zaleplon, for the convulsant drug picrotoxin, for the anticonvulsant barbiturates, and perhaps even for alcohol. This receptor complex is hypothetically responsible in part for mediating such wide-ranging CNS activities as seizures, anticonvulsant drug effects, and the behavioral effects of alcohol, as well as the known anxiolytic, sedative-hypnotic, and muscle relaxant effects of the benzodiazepines. [Pg.313]

In SUMMARY, the naturally occurring ligands for the benzodiazepine and /or GABA-A receptor sites that act as sedative-hypnotics or anxiolytics all directly or indirectly augment GABA-A receptors and thereby depress neuronal activity. In this respect they act in a similar way to the various classes of drugs used to treat anxiety and insomnia. Such compounds do not induce natural sleep. They all increase slow-wave sleep but reduce REM sleep. [Pg.452]


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See also in sourсe #XX -- [ Pg.17 ]




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