Alcohol and Dopamine
Just when you thought you knew it all. Common wisdom says alcohol is a depressant. Wrong. It is so much more.
Alcohol is a small molecule which interacts with many neurotransmitter systems in the brain. The action of alcohol in the brain is very different from and far more complex than large molecules such as opiates, THC, or amphetamines. Key alcohol interactions include the following:
GABA (inhibitory pathway): Alcohol affects the GABA system similar to valium leading to relaxation and drowsiness
Endorphin (the feel-good pathway): Alcohol affects the endorphin system similar to opiates, acting as a pain-killer and giving an endorphin “high”
Glutamate (can be excititory, affects most of brain’s synapses): It is alcohol’s effects on the glutamate system which lead to staggering, slurred speech and memory blackouts.
Dopamine (think reward and pleasure centers): All drugs which lead to dependence appear to affect the dopamine system. Alcohol is part of this picture.
Norepinephrine (the stress hormone): Also known as noradrenalin. Alcohol causes a release of norepinephrine in the brain, acting as a stimulant and not just as a depressant.
Adrenaline (the ‘flight or fight hormone): Alcohol causes the adrenal glands to release adrenaline–alcohol has stimulant properties.
Alcohol does not lead to an increase of dopamine throughout the brain; it only causes an increase in dopamine in the area of the reward pathway (Boileau et al 2003). This reward pathway includes the nucleus accumbens, the VTA (ventral tegmental area) and a portion of the pre-frontal cortex (think executive decision center). Experimental evidence indicates alcohol does not cause the increase in dopamine directly. Alcohol directly affects the GABA system and the endorphin system whereby neurons from the GABA system extend into the reward pathway and when alcohol affects the GABA system these neurons release dopamine into the reward pathway. Subsequently, neurons extend from the endorphin system into the reward pathway and these also release dopamine into the reward pathway when alcohol directly stimulates the endorphin system (Boileau et al, 2003).
All things which give us pleasure can cause a release of dopamine in the reward pathway as well as triggering a number of other events in the brain including endorphin release and activation of the orbitofrontal region of the prefrontal cortex. Researchers from the 1950s implanted electrodes into the reward pathway thought that they had discovered the pleasure center of the brain (Olds, 1956). However, pleasure is a far more complex phenomenon involving many parts of the brain. Modern researchers believe that pleasure has several components such as “liking,” “wanting,” “learning (pavlovian conditioning),” “reward,” and “valuation” (Berridge and Kringelbach, 2008).
It is highly probably dopamine in the reward pathway is involved in the phenomena of “wanting,” “learning,” and “reward,” yet not involved in “liking” or “valuation.” In other words, the dopamine in the reward pathway may make you crave drugs or alcohol or sex or a symphony, and it may also reinforce habitual drug use, sex, or symphony listening. It is not responsible for the pleasure you get from these activities. Interesting enough, the pleasure which we get seems to involve neurotransmitters called endorphins and involves hedonic hot spots. Researchers identify the hedonic hot spots as existing in the Nucleus Accumbens, Ventral Pallidum, and Parabrachial Nucleus. You may recall that the Nucleus Accumbens is also a part of the reward pathway. This hints to us the Nucleus Accumbens is involved in “liking” and part of it is involved in “wanting.” The orbito-frontal (anterior) area of the prefrontal cortex is largely involved in the “valuation” of pleasurable stimuli. The reward pathway is an important survival mechanism for the individual and the species–it fosters learning by rewarding us for actions which result in the acquisition of food or sex. This leads us to learn these behaviors as conditioned responses.
There is also nothing inherently wrong in using alcohol or other drugs to chemically stimulate the hedonic hot spots and the reward pathway. The majority of people who engage in recreational alcohol intoxication or recreational drug use do not become dependent. Key Point: Use caution and try to avoid daily use if we wish to avoid alcohol or drug dependence. It is well known that alcohol has the properties of both a stimulant and a depressant. Alcohol affects many different neurotransmitter systems. However, it is unlikely that the increase in dopamine levels are responsible for the stimulant properties of alcohol. Stimulant properties of cocaine and amphetamine are due to their effect on the dopamine system, yet these drugs differ from alcohol in that they affect dopamine receptors directly and hence have an impact on dopamine receptors throughout the entire brain whereas alcohol affects dopamine receptors indirectly and only in one small part of the brain, namely the reward pathway.
It is most likely that the stimulating effects of alcohol are due to its effects on adrenaline, norepinephrine and the prefrontal cortices. Alcohol causes the release of norepinephrine in the brain (McDougle et al 1995). It also causes the pituitary gland to release hormones which signal the adrenal glands to release adrenaline (NIAAA 1996). Finally, alcohol represses the functioning of the prefrontal cortex (Volkow et al 1990) which is responsible for decision making. This most common effect is why alcohol can cause people to lose their inhibitions and make some really bad decisions while ‘under the influence’.
We should also note that the action of alcohol is biphasic or two-fold: when BAC (blood alcohol concentration) levels are rising, the stimulant properties of alcohol are more pronounced; when BAC levels are falling, the depressant effects of alcohol are more pronounced (Giancola and Zeichner 1997). It is alcohol’s effect on the GABA system which is responsible for its depressant effects, referencing that which slows down the central nervous system. This does not refer to drugs which induce depression. The relationship of alcohol to depression is complex; although alcohol can induce depression in some long term heavy drinkers, Denning and Little (2011) note that alcohol can also function as an antidepressant in some drinkers, particularly women. Ironically, some people with depression use alcohol to escape from it.
Colorado is a state at the fore-front of the THC/CBD revolution (or evolution). We should not forget the millennia of years, however, of alcohol’s use and human co-dependence especially how the molecule affects us no matter how special or limited-edition the label which disguises the product in which it is contained. Oh, and yes – it’s effects on the central nervous system including vision, ocular-motor control, accommodation and general motor function should never be forgotten. Thanks for reading! Warmly,