Disclaimer: I am in no way encouraging substance-use, but we all know that CC students are a curious group of kids, restrained by few laws. Curiosity is a wonderful thing; it led to the discovery of the Americas, the theory of evolution, and modern medicine. However, curiosity also killed the cat. I am presenting the current scientific facts about pharmacological activities so you can make an informed decision before you conduct a single-subject experiment on your personal neurochemistry.

It’s first week and you’re finally out of that cruel and unusual Friday afternoon lab that’s been dragging on forever. First order of business: a margarita at La’au’s. Sometimes getting day drunk on a sunny afternoon seems like best way to decompress. Many CC students feel that alcohol use is part of the college experience.    As a society, we have been educated about the evils of “hard” drugs, yet most of us are under-informed about alcohol.

Our brains contain cells called neurons, which communicate using chemicals called neurotransmitters. Alcohol affects many different neurotransmitter systems and this causes varying effects. Alcohol is considered to be a depressant and it primarily targets the neurotransmitter γ-Aminobutyric acid (GABA). GABA helps to inhibit activity throughout the brain; it’s the chemical that makes you feel sleepy and relaxed at night.

Alcohol acts like GABA but lasts a lot longer and has a stronger effect than the naturally occurring neurotransmitter. This is one of the reasons that drinkers feel relaxed and uninhibited. GABA neurons are found in the prefrontal cortex (decision making), hippocampus (memory), and cerebellum (coordination). That’s why you don’t remember falling while trying to twerk on the bar at 927.

The increase in GABA has downstream repercussions as well. Glutamate, the main excitatory neurotransmitter in our brains is also effected.  NMDA receptors, one of the receptors that pick up glutamate, become more sensitive when the brain is widely inhibited for long periods of time, like a long night or weekend of drinking. When the brain is no longer inhibited, NMDA receptors can become overwhelmed and this can lead to cell death. There are lots of NMDA receptors in parts of the brain involved in learning and memory, such as the hippocampus.

Alcohol is interesting because, as BAC increases, it causes the drinker to feel awake, chatty, and prone to breaking exit signs. This occurs because alcohol initially causes an increase in norepinephrine, a neurotransmitter that increases alertness and impulsivity. This is the reason that alcohol makes you feel excited and enthusiastic about braving the increasingly cold nights to venture to a house party.

In addition to norepinephrine, endorphins and dopamine are also released in the brain when you have that first PBR of the night. These chemicals are the brain’s pleasure chemicals; endorphins dull the perception of pain (hello alcohol jacket). Dopamine is part of you brain’s reward system and it produces the euphoric rush that comes right after you take a shot of seemingly disgusting cheap liquor. Dopamine is the chief culprit in addiction; you continue to drink in order to reinforce that euphoria until you land yourself a one-way ticket to Boettcher.

As a society, we often use moral reasons to deter people from drinking. It’s entirely possible to avoid the classically negative consequences of alcohol (drunk driving, alcohol poisoning, full blown alcoholism) yet still experience negative cognitive effects. Moral of the story: when it comes to alcohol, be informed, but moderation is probably the best policy.

Elle Beckett, Guest Writer

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