The holidays are upon us, and that means there is a high probability that you will soon come into contact with someone who is blackout drunk. Or maybe it is you who will end up in this state. Either way, the experience may leave you wondering why heavy drinking has this effect on our brains.
Since we here at IFLScience love answering life’s strange questions, let’s dive on in.
According to insights from the latest research on the subject, alcohol-induced amnesia is theorized to occur because alcohol, which can cross the blood-brain barrier, interferes with a receptor found on neurons involved in memory formation. The inhibitory process – first identified in the early 1990s but still not fully understood – unfolds when ethanol finds its way to the pyramidal neurons within the CA1 region of the hippocampus. Pyramidal neurons are a type of nerve cell with many dendrites but only one axon, and thus serve to receive information from other cells before sending one integrated signal onward. The CA1 hippocampus region is known to be a site of long-term potentiation (LTP), the process by which the synapse joining two neurons becomes more sensitive to stimulation as a result of the two neurons communicating frequently. The mechanism underlying LTP itself also remains quite mysterious, yet scientists do know that the phenomenon is crucial to memory formation.
In a 2011 study, published in The Journal of Neuroscience, lead investigator Dr Charles Zorumski and his colleagues used experiments in rats to tease out more detail of ethanol’s effects. They determined that alcohol blocks LTP by messing with the N-methyl-D-aspartate (NMDA) receptor on CA1 pyramidal neurons, causing them to release steroids that inhibit neuron plasticity. And no neural plasticity means no changing synaptic connections, and therefore no memory formation.
“It takes a lot of alcohol to block LTP and memory,” Dr Zorumski said in a past statement. “But the mechanism isn’t straightforward. The alcohol triggers these receptors to behave in seemingly contradictory ways, and that’s what actually blocks the neural signals that create memories. [This finding] may explain why individuals who get highly intoxicated don’t remember what they did the night before.”
He explains that copious alcohol appears to block some NMDA receptors while activating others. His group’s insights counter the long-held notion that alcohol impairs memory by simply killing brain cells.
“Alcohol isn’t damaging the cells in any way that we can detect,” Zorumski added. “As a matter of fact, even at the high levels we used here, we don’t see any changes in how the brain cells communicate. You still process information. You’re not anesthetized. You haven’t passed out. But you’re not forming new memories.”
Past research has shown that acute stress can also impair LTP, though the process is actually boosted immediately following the threatening event, when corticosteroid hormones involved with the physiological stress response are still high (which makes sense from an evolutionary perspective because animals need to remember and learn from threats they encounter). Some evidence also suggests that long-term stress interferes with memory as well, likely also through suppressed LTP.
Though most of this work has been done in animals, it is predicted to work the same in humans, meaning that there is a decent probability that if you consume copious amounts of booze or get anxious – essentially two holiday season traditions, often found together – your brain’s ability to store new information will be compromised. Good luck getting through the month, everyone.
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