How drinking can literally change the ‘Shape of You’: Effect of alcohol on neuronal structure of the brain
By Sharvari Ajit Deepti Narendra, Bioinformatics, 2020
When people think of alcohol, their mind might remember the last time they were drunk — the low glutamate levels causing their thought process to slow down, the increased gamma-Aminobutyric acid (GABA) levels causing drowsiness, and the waves of dopamine crashing inside the brain, maintaining the high. In simple words, they remember feeling good about themselves for having drunk dialed their exes and slurring their feelings on the phone. Yet, they also remember going into a depressive state, caused by the same increased dopamine levels, and crying over either their actions or unreciprocated feelings. Because dopamine causes simultaneous highs and lows, the brain keeps getting tricked into feeling great, causing people to continue drinking until they pass out or, in some cases, even black out. This constitutes the other half of people who remember getting drunk, but do not remember what happened after.
There have been various established studies illustrating the effect of alcohol on chemicals, like dopamine, that are released by neurons in the brain (i.e. neurotransmitters). Now, scientists are interested in knowing how alcohol affects the neuron’s structure itself. A study published in December 2019 by Claudia Aghaie et al. demonstrated that rats exposed to alcohol (ethanol) before birth showed a decrease in dopaminergic neuron body size in the ventral tegmental area (VTA) of the brain. The VTA is an integral part of the reward system of the brain — the same system that keeps tricking people into feeling great after drinking alcohol, despite making rash decisions like having unprotected sex or driving while being intoxicated. Alcohol activates the dopaminergic (dopamine transmitting) neurons in the VTA, which causes increased dopamine levels in the nucleus accumbens (NAc), another integral component of the reward system.
Alcohol activates the dopaminergic (dopamine transmitting) neurons in the ventral tegmental area, which causes increased dopamine levels in the nucleus accumbens (NAc), another integral component of the reward system.
The NAc also receives spiny projection neurons, known as striatal medium spiny neurons (MSNs), which produce GABA, the primary inhibitory neurotransmitter. The drowsiness caused by increased GABA production owing to drinking alcohol is because of the inhibitory nature of this chemical — it inhibits impulses in the neuron so that it does not excite nearby neurons as well. A study published in 2015 by Texas A&M Health Science Center College of Medicine showed that drinking alcohol leads to changes in the structure of MSNs located in the dorsomedial striatum, the area of the brain responsible for selecting an action based on expected reward value or the selection of a goal-directed action. This means that if people want to keep feeling good after drinking alcohol, the dorsomedial striatum assists in their decision to drink more. In other words, as the old saying goes: “First you take a drink, then the drink takes a drink, then the drink takes you.”
In the NAc, on the other hand, small protrusions from these MSNs, known as dendritic spines, serve as receptor sites for both dopaminergic and glutamatergic (glutamate transmitting) neurons originating from other regions of the brain, and together they display an unusual form of arrangement called the “synaptic triad.” Alcohol addiction is thought to affect the architecture of this structure by changing the head sizes of the dendritic spines.
They demonstrated that dopamine administration to rats undergoing alcohol withdrawal reversed the change in the synaptic architecture in the NAc.
Withdrawal from alcohol addiction, the symptoms of which can be even worse than being addicted to alcohol in the first place, is also shown to remodel the architecture of the synaptic triad. Additionally, previous research in 2014 by Spiga et al. on withdrawal has witnessed reductions in dopaminergic projections to the triad. A study conducted in the beginning of 2019 by a group of scientists from University of Palermo in Italy used the results from this previous study to their advantage. Since alcohol withdrawal showed reduced dopaminergic transmissions along with changes in the synaptic triad structure, they decided to investigate the effect of boosting dopamine signaling on the triad architecture. They demonstrated that dopamine administration to rats undergoing alcohol withdrawal reversed the change in the synaptic architecture in the NAc, and they proposed the possibility of boosting dopamine signaling as a therapeutic measure for alcohol-related dysfunction.
Alcohol consumption and dependence is a vast area of study that is slowly branching towards investigating alcohol-induced neuronal structural variations. More research is needed to explore if changes in neuronal structures can be targeted for alcohol treatment and if similar changes are observed in humans as well. Until then, here’s to hoping that, like Tyrion Lannister, we would also drink and know things.
Alcoholism: Clinical and Experimental Research (2019). Doi: 10.1111/acer.14275.
The Journal of Neuroscience (2019). Doi: 10.1523/JNEUROSCI.1377–18.2018.
