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In pharmacology, GABA A receptor positive allosteric modulators, also known as GABAkines or GABA A receptor potentiators, [1] are positive allosteric modulator (PAM) molecules that increase the activity of the GABA A receptor protein in the vertebrate central nervous system. GABA is a major inhibitory neurotransmitter in the central nervous system.
The gabapentinoids are 3-substituted derivatives of GABA; hence, they are GABA analogues, as well as γ-amino acids. [3] [4] Specifically, pregabalin is (S)-(+)-3-isobutyl-GABA, phenibut is 3-phenyl-GABA, [28] and gabapentin is a derivative of GABA with a cyclohexane ring at the 3 position (or, somewhat inappropriately named, 3-cyclohexyl-GABA).
Alcohol is another substance that often cross-tolerates with other drugs. Findings of cross-tolerance with nicotine in animal models suggest that it is also possible in humans, and may explain why the two drugs are often used together. [6] Numerous studies have also suggested the possibility of cross-tolerance between alcohol and cannabis. [7]
The ionotropic GABA A receptor protein complex is also the molecular target of the benzodiazepine class of tranquilizer drugs. Benzodiazepines do not bind to the same receptor site on the protein complex as does the endogenous ligand GABA (whose binding site is located between α- and β-subunits), but bind to distinct benzodiazepine binding sites situated at the interface between the α- and ...
The transporter and its effect on GABA concentrations in the amygdala has been implicated as a key player in the disease of alcoholism. In studies conducted on rat populations, reduction of GAT3 caused rats who formerly preferred sugar to prefer alcohol. Further, studies of deceased alcoholics show a decreased concentration of GAT3 in their brains.
[1] [2] The effects of GABA A receptor NAMs are functionally the opposite of those of GABA A receptor positive allosteric modulators (PAMs) like the benzodiazepines, barbiturates, and ethanol . [1] [2] Non-selective GABA A receptor NAMs can produce a variety of effects including convulsions, neurotoxicity, and anxiety, among others. [1] [2]
Fast-responding GABA receptors are members of a family of Cys-loop ligand-gated ion channels. [7] [8] [9] Members of this superfamily, which includes nicotinic acetylcholine receptors, GABA A receptors, glycine and 5-HT 3 receptors, possess a characteristic loop formed by a disulfide bond between two cysteine residues. [10]
Gabapentin at a low dose of 100 mg has a T max (time to peak levels) of approximately 1.7 hours, while the T max increases to 3 to 4 hours at higher doses. [85] Food does not significantly affect the T max of gabapentin and increases the C max and area-under-curve levels of gabapentin by approximately 10%. [93]