What happens in your brain when you get blacked-out drunk?

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SUMMARY

The discussion centers on the neurological effects of alcohol consumption, particularly regarding blackouts. Alcohol significantly impacts NMDA receptors, which are crucial for memory formation in the hippocampus, leading to impaired long-term potentiation (LTP). This disruption results in the inability to form memories during episodes of high intoxication. Additionally, individual differences in alcohol metabolism contribute to the likelihood of experiencing blackouts, as not everyone processes alcohol in the same way.

PREREQUISITES
  • Understanding of NMDA receptors and their role in memory formation
  • Knowledge of long-term potentiation (LTP) and its significance in learning
  • Familiarity with alcohol metabolism and its effects on the brain
  • Basic concepts of cognitive neuroscience
NEXT STEPS
  • Research the effects of NMDA receptor antagonists on memory and cognition
  • Study the process of long-term potentiation (LTP) in synaptic connections
  • Explore the biochemical pathways of alcohol metabolism, including the roles of alcohol dehydrogenase and acetaldehyde dehydrogenase
  • Read "Under the Influence" by James R. Milam for insights into alcohol's effects on the brain
USEFUL FOR

This discussion is beneficial for cognitive neuroscientists, psychologists, addiction specialists, and individuals seeking to understand the cognitive effects of alcohol consumption and memory impairment.

Jamin2112
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Lots of us have drank to the point where, the following day, we didn't remember a significant portion of the night prior. What happens in our brain? Does it not record memories after a certain blood-alcohol level or does it put those memories in the back storage of our brain, where they can't be accessed? Weirdest thing ever. I dare say I probably had over 50 blacked-out episodes when I lived in my fraternity.
 
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It's thought to be due to the effect of alcohol on NMDA receptors (which generally reside on the post-synaptic cell in a synaptic connection between two cells and plays a large role in memory formation in the hippocampus.)

alcohol interferes with key receptors in the brain, which in turn manufacture steroids that inhibit long-term potentiation (LTP), a process that strengthens the connections between neurons and is crucial to learning and memory.

It gets more complicated, you can read the rest here if you're interested in the details:

http://news.wustl.edu/news/Pages/22479.aspx
 
I dare say I probably had over 50 blacked-out episodes when I lived in my fraternity

Yes, this level of alcohol use tends to create a syndrome who's technical name is abbreviated CRS. While there may be some receptor and steriod action going on that attenuates memory consolidation, the real issue with black-outs is what is going on WHILE you are blacked-out and walking around blind-stinking Neanderthal drunk. There is some thinking that the more recently evolved lateral frontal cotical function is compromised in this instance.
 
I really, really, really suggest you get a copy of this book.
http://www.barnesandnoble.com/w/under-the-influence-james-r-milam/1102541472

Its early chapters explain in simple terms the processs by which we metabolize alcohol.
It explains chemical actions going on in the brain while digesting alcohol.
If you ever took differential equations and worked rate problems that chapter will really strike home, but it's not necessary that you have any math at all.

In a nutshell - Not everybody digests alcohol the same.
Blackouts are a strong clue that an individual might have a digestive process for alcohol that leads to problems. Many people don't get blackouts.

We don't diagnose here in PF.
This is a friendly word of advice from somebody who's been there.
Educate yourself on this matter.

old jim
 
This is a friendly word of advice from somebody who's been there.

You must be on the wagon, Jim, to have received the PF 2012 engineering award. Good for you. One day at a time, brother...

Here's a trivia question, which I'll answer myself if I don't get a correct answer within 20 min.

How does anti-buse work? And no Googling!
 
Alright, I gave you a chance. I think that alcohol dehydrogenase forms acetaldehyde, which acetaldehyde dehydrogenase metabolizes. Anti-buse blocks the action of acetaldehyde dehydrogenase which makes you feel waaaay sick. Although thankfully I don't speak from experience.
 
Hey Dirac, Thanks for the kind words !

Your description of Antabuse sounds a lot like what i read in that book linked above nearly 30 years ago. So i think you're probably right on. Friends who drank on antabuse say it gives an awful headache, which sounds to me like aldehyde of some sort..
I never had antabuse either.

I don't want to push the limit of this rule,
""Refrain from disclosing personal information.""
so just let me say yes I'm on the wagon since ~'88 timeframe.
Everybody has their own story. Mine involves Bill W and Dr Bob, William Bouguereau and Carl Jung. Jung helped Bob Smith develop the process, as you know.

......back to topic:
Jamin asked:
Does it not record memories after a certain blood-alcohol level...
I'm not sure whether it's the actual ethanol level or one of the intermediate chemicals it turns into along its metabolic journey to sugar. Probably the latter, since not all people get blackouts and not all people metabolize ethanol the same. Milam and Ketcham's book has information about that phenomenon, too. They say the events are just not recorded into memory.

old jim
 
My field is cog neuroscience and I think that alcohol compromises frontal lobe function, which is why you black out...but I'm too lazy to research it right now, hehe.

I think the best high I ever had, though, is a good dose of mathematical physics, it never let's you down.
 

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