Alcohol Use Disorder

Alcohol Use Disorder (AUD) is a medical condition characterized by a pattern of excessive drinking that interferes with a person's daily life. AUD ranges from mild to severe and can lead to a range of physical, psychological, and social problems.

Some common symptoms of AUD include:

Craving alcohol Inability to stop or limit drinking Withdrawal symptoms when not drinking, such as anxiety, shaking, or nausea Building up a tolerance to alcohol, so that you need more to feel the effects Drinking in hazardous situations, such as while driving or operating heavy machinery Neglecting responsibilities at work, school, or home Continuing to drink even though it is causing problems in relationships Giving up activities you once enjoyed in order to drink Drinking more than intended or for longer periods of time If you think you may have AUD, it's important to seek help from a healthcare provider or mental health professional. They can diagnose and treat the condition, and help you develop a plan for recovery. Treatment options for AUD may include behavioral therapy, medication, or a combination of both. Support from friends, family, or support groups, such as Alcoholics Anonymous, can also be helpful in recovery

Persons at risk for developing alcohol use disorder (AUD) differ in their sensitivity to acute alcohol intoxication. Alcohol effects are complex and are thought to depend on multiple mechanisms. Harmata et al. explored whether acid-sensing ion channels (ASICs) might play a role. They tested ASIC function in transfected CHO cells and amygdala principal neurons and found alcohol-potentiated currents mediated by ASIC1A homomeric channels, but not ASIC1A/2 A heteromeric channels. Supporting a role for ASIC1A in the intoxicating effects of alcohol in vivo, they observed marked alcohol-induced changes on local field potentials in the basolateral amygdala, which differed significantly in Asic1a-/- mice, particularly in the gamma, delta, and theta frequency ranges. Altered electrophysiological responses to alcohol in mice lacking ASIC1A, were accompanied by changes in multiple behavioral measures. Alcohol administration during amygdala-dependent fear conditioning dramatically diminished context and cue-evoked memory on subsequent days after the alcohol had cleared. There was significant alcohol-by-genotype interaction. Context- and cue-evoked memory were notably worse in Asic1a-/- mice. They further examined the acute stimulating and sedating effects of alcohol on locomotor activity, loss of righting reflex, and an acute intoxication severity scale. They found loss of ASIC1A increased the stimulating effects of alcohol and reduced the sedating effects compared to wild-type mice, despite similar blood alcohol levels. Together these observations suggest a novel role for ASIC1A in the acute intoxicating effects of alcohol in mice. They further suggest that ASICs might contribute to the intoxicating effects of alcohol and AUD in humans ¹⁾