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This presents a novel indirect mechanism and suggests that a metabolite, not the ethanol itself, could cause the behavioural or symptomatic effects of alcohol intoxication. Many of the primary targets of ethanol are known to bind PIP 2 including GABA A receptors, [30] but the role of PEth needs to be investigated further.
Besides giving GABA receptors an extra inhibitory punch, alcohol substrates bind to glutamate receptors, which blocks its excitatory activity. Alcohol effects on both of these metabolic pathways obstruct the brain from making memories, making well thought out decisions, and controlling impulses after long term use.
Acute alcohol intoxication through excessive doses in general causes short- or long-term health effects. NMDA receptors become unresponsive, slowing areas of the brain for which they are responsible. Contributing to this effect is the activity that alcohol induces in the gamma-aminobutyric acid (GABA) system. The GABA system is known to inhibit ...
Ethanol binding to GABA A receptor. Alcohol works in the brain primarily by increasing the effects of γ-Aminobutyric acid (GABA), [256] the major inhibitory neurotransmitter in the brain; by facilitating GABA's actions, alcohol suppresses the activity of the CNS. [256]
Ethanol (alcohol) has a very similar mechanism of tolerance and withdrawal to benzodiazepines, involving the GABA A receptors, NMDA receptors and AMPA receptors, but the majority of research into kindling has primarily focused on alcohol. [6] An intensification of anxiety and other psychological symptoms of alcohol withdrawal also occurs. [10]
A subclass of ionotropic GABA receptors, insensitive to typical allosteric modulators of GABA A receptor channels such as benzodiazepines and barbiturates, [27] [28] [29] was designated GABA ะก receptor. [30] [31] Native responses of the GABA C receptor type occur in retinal bipolar or horizontal cells across vertebrate species. [32] [33] [34] [35]
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 ...
[9] [10] One of alcohol's primary effects is the allosteric inhibition of NMDA receptors and facilitation of GABA A receptors (e.g., enhanced GABA A receptor-mediated chloride flux through allosteric regulation of the receptor). [11] At high doses, ethanol inhibits most ligand gated ion channels and voltage gated ion channels in neurons as well ...