page_title: Alcohol intoxication
section_title: GABAA receptors
hierarchical_section_title: Alcohol intoxication / Pathophysiology / GABAA receptors
caption_attribution_description: English: Ethanol binding to GABA Receptor
context_page_description: Alcohol intoxication, also known as drunkenness or alcohol poisoning, is the negative behavior and physical effects due to the recent drinking of alcohol. Symptoms at lower doses may include mild sedation and poor coordination. At higher doses, there may be slurred speech, trouble walking, and vomiting. Extreme doses may result in a respiratory depression, coma, or death. Complications may include seizures, aspiration pneumonia, injuries including suicide, and low blood sugar. Alcohol intoxication can lead to alcohol-related crime with perpetrators more likely to be intoxicated than victims.
  Alcohol intoxication typically begins after two or more alcoholic drinks. Risk factors include a social situation where heavy drinking is common and a person having an impulsive personality. Diagnosis is usually based on the history of events and physical examination. Verification of events by witnesses may be useful. Legally, alcohol intoxication is often defined as a blood alcohol concentration of greater than 5.4–17.4 mmol/L. This can be measured by blood or breath testing. Alcohol is broken down in human body at a rate of about 3.3 mmol/L per hour.
context_section_description: Many of the effects of activating GABAA receptors have the same effects as that of ethanol consumption. Some of these effects include anxiolytic, anticonvulsant, sedative, and hypnotic effects, cognitive impairment, and motor incoordination. This correlation between activating GABAA receptors and the effects of ethanol consumption has led to the study of ethanol and its effects on GABAA receptors. It has been shown that ethanol does in fact exhibit positive allosteric binding properties to GABAA receptors. However, its effects are limited to pentamers containing the δ-subunit rather than the γ-subunit. GABAA receptors containing the δ-subunit have been shown to be located exterior to the synapse and are involved with tonic inhibition rather than its γ-subunit counterpart, which is involved in phasic inhibition. The δ-subunit has been shown to be able to form the allosteric binding site which makes GABAA receptors containing the δ-subunit more sensitive to ethanol concentrations, even to moderate social ethanol consumption levels (30mM). While it has been shown by Santhakumar et al. that GABAA receptors containing the δ-subunit are sensitive to ethanol modulation, depending on subunit combinations receptors, could be more or less sensitive to ethanol. It has been shown that GABAA receptors that contain both δ and β3-subunits display increased sensitivity to ethanol. One such receptor that exhibits ethanol insensitivity is α3-β6-δ GABAA. It has also been shown that subunit combination is not the only thing that contributes to ethanol sensitivity. Location of GABAA receptors within the synapse may also contribute to ethanol sensitivity.
caption: Ethanol binding to GABAA receptor
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