Also known as ethyl alcohol or drinking alcohol. Ethanol is a centrally acting depressant best known as the primary constitutent in alcoholic beverages. It has sedative-hypnotic, muscle relaxant, anticonvulsant, anaesthetic and analgesic properties.
Alcohol is the most popular and widely used psychoactive known. Despite its habit forming, highly toxic, and impairing properties, Its use is well accepted in most social circles. Alcoholic beverages are consumed recreationally throughout most countries of the world. These beverages are a staple of many cultures and are commonly classified into three categories; beer, wine, or spirits.
The effects of alcohol are dose dependent, and have been popuarly gauged on a scale of blood alcohol concentration (i.e. BAC).
Alcohol produces effects which range from euphoria, excitement and social disinhibition (increased sociability) in lower doses; to relaxation, anxiolysis, impaired judgement and drowsiness in moderate doses; to sedation or hypnosis, sensory and motor impairment, analgesia, anaesthesia, unconsciousness, coma, respiratory depression and death in higher doses.
Its effects are similar in nature to other CNS depressants such as benzodiazepines and barbiturates, although it shares other properties with dissociatives such as ketamine or PCP.
Generally speaking, alcohol produces predominantly depressant effects on the central nervous system through its action on multiple systems of neurotransmission. Like other sedatives, it can reduce arousal of the HPA axis and sympathetic nervous system. It affects many areas of the brain, including (in general terms) the cerebral cortex, midbrain, and brainstem, depending on the dose.
Ethanol enhances the action of the GABA-ergic inhibitory system, acting as a positive allosteric modulator at the GABA-A receptor - GABA-A is the primary inhibitory receptor subtype of the CNS and is targeted by barbiturates and benzodiazepines as well.
Ethanol is an NMDA antagonist - i.e. it blocks the excitatory NMDA receptor, inhibiting the transmission of the neurotransmitter glutamate. In the higher, often toxic, dose range, ethanol inhibits AMPA receptors as well - the AMPA receptor is also a glutamatergic receptor.
Ethanol potentiates the nicotinic acetylcholine receptor. Being an excitatory circuit, its pro-cholinergic activity is certainly not involved in mediating its depressant effects. However, anticholinergic agents have been shown to reduce alcohol induced mesolimbic excitatory activity.
On a different note; the euphoric, rewarding, and reinforcing effects of alcohol (associated with the limbic system) have been linked with an increase in morphinomimetic or endogenous opioid activity. Furthermore, there seems to be a complex working relationship between the catecholaminergic and serotonergic systems in these areas with the opioid system.
Alcohol is metabolized in the liver by oxidation, carried out by alcohol dehydrogenase. Its metabolism differs from other drugs in that it is eliminated at a constant rate - as opposed to having an exponential half life. In fact, alcohol is metabolized at a slower rate than it is absorbed - therefore, it is extremely important that drinkers pace themselves. Typically no more than 1 drink an hour.
Following a standard drink, peak plasma concentrations occur after 30-45 minutes.
Its breakdown is as follows: alcohol to acetaldehyde, acetaldehyde to acetic acid, acetic acid to carbon dioxide & dihydrogen monoxide.
Acetaldehyde, its first order metabolite, is believed to be responsible for hangovers.