October 9, 2018
Written by: Carolyn Keating
It’s happened to most of us before: you’re at a party surrounded by people you don’t know, but luckily there’s that social lubricant, booze. Soon you’re less anxious, chattier, and feeling good. Hopefully you don’t drink so much that you start stumbling or have trouble remembering things. Alcohol can certainly alter us in many ways, but how exactly does that happen?
Many people have heard that alcohol is a depressant—a drug that reduces neuronal activity. But it’s not quite so simple. Alcohol affects almost all of the neurotransmitter systems in the brain, leading to the large range of behaviors that can occur when someone is buzzed or drunk. Let’s take a closer look at the neuroscience behind some of the “symptoms” of alcohol use:
One reason people might drink is to unwind from a long day or to decrease stress in social situations. As little as one or two drinks can have strong anxiety-relieving effects. These changes are due to the brain’s foremost inhibitory neurotransmitter, GABA. Low amounts of alcohol can enhance the effects of GABA at some of its receptors, particularly one known as the GABAA receptor1. Making GABA more responsive at its receptors is the same way drugs such as benzodiazepines reduce anxiety. But where does this reduction in neuronal firing occur to relieve anxiety? Studies in rodents have shown that alcohol increases GABA-mediated inhibition of neuronal activity in a brain region called the basolateral amygdala, which plays a large role in controlling anxiety-like behavior2. Other studies in humans have shown that under the influence of alcohol, the amygdala and other brain regions involved in emotional processing are less active than normal when subjects are shown fearful/angry faces3. This inability to distinguish threatening stimuli may also contribute to alcohol’s anxiety-reducing effects.
Alcohol does more than just take away a bad feeling; it’s also actively rewarding, just like other drugs of abuse. Alcohol affects the serotonin, dopamine, and opioid neurotransmitter systems in the brain, all of which are involved with reward pathways1. Unlike its anxiety relieving effects, produced by dampening neuronal activity, here alcohol leads to rewarding feelings by increasing activity in distinct regions of the brain. This increase in activity was found using positron emission tomography, or PET scans. Here, participants are given a small amount of radioactive material that can be detected on a scanner. This radioactive material is usually glucose, which is taken up as fuel by cells that are active. Using this technique, scientists have been able to see which regions of the brain are active in the presence of alcohol, based on which areas show an increase in uptake of this radioactive glucose fuel. They have found that alcohol causes an increase in glucose usage in a variety of areas involved with incentive and motivation in drug reward. Furthermore, another group found an increase of dopamine in the ventral striatum, one of the region associated with reward and motivation4. These studies show us that alcohol isn’t globally depressing all neuronal activity; it’s actually increasing activity in the brain’s reward centers, making us feel good.
While alcohol may increase the activity of brain regions involved with reward, it decreases the activity of virtually every other brain region, which is why it’s known as a depressant. Because of this duality, it is thought that alcohol results in poor decision-making by promoting reward-seeking behavior, while depressing behaviors that rely on higher-level cognitive processes, like inhibiting responses and monitoring errors.
Let’s take risky behavior as an example. In order to look at which regions are involved with making risky choices under the influence of alcohol, researchers have used functional magnetic resonance imaging (fMRI), which measures the amount of blood flow or oxygen to different regions of the brain as a proxy for neuronal activity. Subjects were given alcohol via IV, and then asked to play a game where they could make safe or risky choices. With the safe choices, subjects were guaranteed to win a little money. With the risky choices they could potentially win a greater amount of money, but they could also possibly lose money. When subjects were given alcohol, they made more risky choices, and showed increased activation in the striatum (reward center) when they made risky compared with safe choices. Interestingly, alcohol decreased the neuronal response to notification of the outcome of the game, meaning the brain didn’t pay attention to whether they won or lost. This study suggests that alcohol may increase risk-taking behavior by activating brain regions involved in reward when a decision is made, while not caring about the outcomes of that decision5. And maybe that’s why drunkenly texting your ex only seems like a good idea at the time.
Alcohol also impacts the ability to monitor your own behavior for errors. For instance, subjects were orally given alcohol and asked to complete a Go/No‐Go task, where they were required press a button as quickly as possible when they saw the letter “X,” but not press the button when they saw the letter “K.” With alcohol, participants had longer reaction times and more errors (both pressing when not supposed to, and not pressing when they should have). fMRI showed that a region of the brain called the anterior cingulate cortex (ACC) was less active when subjects accidently button-pressed when they weren’t supposed to. These results suggest that alcohol may impair monitoring one’s own behavior by suppressing the ACC6.
There’s a reason police officers ask suspected drunk-drivers to walk a straight line or touch their hand to their nose when performing field sobriety tests: lack of muscle coordination (ataxia) is a prominent effect of even low amounts of alcohol consumption. Alcohol has strong effects on a brain region called the cerebellum, an important area for controlling and coordinating movements. PET and fMRI studies have consistently found decreased neuronal activity in this region after alcohol consumption4. Via the enhanced GABA inhibitory signaling mentioned at the beginning of the article, alcohol causes a decrease in firing of the cells in the cerebellum responsible for controlling movements7.
Large amounts of alcohol, especially when consumed rapidly, can cause someone to not be able to remember key details of events or even entire events. These blackouts are the result of alcohol disrupting the activity of a brain region heavily involved with memory: the hippocampus. Work in rodents has shown that alcohol prevents cells in a certain region of the hippocampus from firing, inhibiting the formation of new memories. The formation of new memories in the hippocampus is reliant on the brain’s excitatory neurotransmitter, glutamate. Alcohol prevents one of glutamate’s receptors—the NMDA receptor—from activating, thus preventing new memories from being formed. Not only does alcohol inhibit the hippocampus itself, but it also impairs the ability of the hippocampus to communicate with other regions of the brain8. Together, all of these actions contribute to the experience of blackouts.
These were just a few examples of how alcohol can alter our behavior. Even from this short list, it’s clear that alcohol can affect many regions of the brain and many of its neurotransmitter systems. Alcohol can certainly have positive effects: it makes us a little braver or less inhibited. But it can also be dangerous, making us more likely to forget things or hurt ourselves (or others! Never drink and drive!). Plus, those positive effects of alcohol can quickly lead to dependence, so always remember to please drink responsibly.
- Eckardt, M. J. et al. Effects of moderate alcohol consumption on the central nervous system. Alcohol. Clin. Exp. Res. 22, 998–1040 (1998).
- Silberman, Y. et al. Neurobiological mechanisms contributing to alcohol-stress-anxiety interactions. Alcohol 43, 509–519 (2009).
- Sripada, C. S., Angstadt, M., McNamara, P., King, A. C. & Phan, K. L. Effects of alcohol on brain responses to social signals of threat in humans. Neuroimage 55, 371–380 (2011).
- Bjork, J. M. & Gilman, J. M. The effects of acute alcohol administration on the human brain: Insights from neuroimaging. Neuropharmacology 84, 101–110 (2014).
- Gilman, J. M., Smith, A. R., Ramchandani, V. A., Momenan, R. & Hommer, D. W. The effect of intravenous alcohol on the neural correlates of risky decision making in healthy social drinkers. Addict. Biol. 17, 465–478 (2011).
- Anderson, B. M. et al. Functional Imaging of Cognitive Control During Acute Alcohol Intoxication. Alcohol. Clin. Exp. Res. 35, 156–165 (2010).
- Mameli, M., Botta, P., Zamudio, P. A., Zucca, S. & Valenzuela, C. F. Ethanol decreases Purkinje neuron excitability by increasing GABA release in rat cerebellar slices. J. Pharmacol. Exp. Ther. 327, 910–917 (2008).
- White, A. M. What happened? Alcohol, memory blackouts, and the brain. Alcohol Res. Health 27, 186–96 (2003).