The blockbuster comedy The Hangover
centered on the drunken misadventures of
a groom-to-be, his groomsmen’s and the hilarious attempt to find him after somehow
getting lost at his own bachelor party. Most who saw it thought it was a really funny
movie in a twisted kind of way.
But even if you didn’t see this particular movie (or its less-than-stellar sequel), we've all witnessed something similar – the person at the party who has had far too much to drink yet can dance up a storm, make witty conversation, or even–heaven forbid–drive a car. But the next morning they have no recollection of their crazy stunts. This lack of recall is known as a “blackout” and is actually amnesic episodes that can last from just a few minutes to much longer.The science behind blackouts.
Now, neuroscientists at Washington University School of Medicine in St. Louis have found the cause of these blackouts by pinpointing the brain cells involved and the molecular mechanism going on. As it turns out, this mechanism is much different than what was previously accepted as fact.
While most of us have always been taught that excessive amounts of alcohol can kill brain cells (remember high school health class?), the new study shows this is not the case. What actually happens is a type of interference
. Alcohol short-circuits key receptors in the brain, which results in these receptors making steroids. These steroids squelch long-term potentiation (LTP), a process that lends to strong connections between brain cells and is essential to learning and memory.
Dr. Yukitoshi Izumi, PhD, research professor of psychiatry at Washington University School of Medicine in St. Louis, says, “The mechanism involves NMDA receptors that transmit glutamate, which carries signals between neurons. An NMDA receptor is like a double edge sword because too much activity and too little can be toxic. We found that exposure to alcohol inhibits some receptors and later activates others, causing neurons to manufacture steroids that inhibit LTP and memory formation.”It takes a lot of alcohol to block LTP and memory.
The brain cells affected by alcohol were found in the hippocampus, an area of the brain known to be important in cognitive function. By studying slices of a rat brain hippocampus, scientists were able to determine that with moderate amounts of alcohol, LTP was unaffected. But when the brain cells were exposed to large amounts the memory formation mechanism was inhibited. Alcohol causes these receptors to behave in ways that block the neuron signals that create memories. This may partly explain why people who get rip roaring drunk don't remember what they did the night before.Your brain on alcohol.
Researchers are quick to point out that brain cell death by alcohol does not lead to blackouts. The neurons aren't killed
but the manufactured steroids play interference with the synapses’ ability to bend and mold so they can connect and communicate. This leads to impaired LTP and memory formation.
All of this flies in the face of everything we thought we knew about the brain and alcohol. Dr. Charles F. Zorumski says, “Alcohol isn't damaging the cells in any way that we can detect. As a matter of fact, even at the high levels we used here, you 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.”This new information could lead to strategies for memory improvement.
Researchers also discovered if they could keep neurons from making steroids, then they could preserve the LTP in the rat hippocampus. They were able to do that with certain drugs called 5–alpha–reductase inhibitors. These drugs actually seemed to preserve memory.
The future goal is to determine if these drugs or others could potentially play a role in preserving memory. In the meantime, while it's nice to know a wild night of partying isn’t killing any brain cells, too much alcohol can have a detrimental effect on your ability to recall–not just the morning after but in the long run as well.
Not to mention what it’s doing to your liver . . .