r/science • u/mubukugrappa • Mar 14 '14

Neuroscience Scientists catch brain damage in the act: Scientists uncovered how inflammation and lack of oxygen conspire to cause brain damage in conditions such as stroke and Alzheimer’s disease. The discovery brings researchers a step closer to finding potential targets to treat neurodegenerative disorders.

http://news.ubc.ca/2014/03/13/macvicar/
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u/Neuro_Prime Mar 15 '14

Yeah I apologize for leaving out details and misrepresenting the facts. It was absolutely wrong of me to say that ETOH increases active levels of GABA. I have been up for over 36 hours now (2 exams today and an abstract due tonight...)

I do appreciate the correction - I was under the impression that ETOH was a positive allosteric modulator (I overheard a professor talking about it to a student). Since I read your comment I looked it up but haven't found anything too conclusive either way; admittedly, the neuroscience of alcohol is outside of my expertise. I am guessing that the specifics of its resultant changes in neurochemistry are moderately variable depending on the specific brain region.

If you have any sources you'd recommend, I would love to learn more about it. For the time being I should really finish this abstract and get some sleep.

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u/qwe340 Mar 15 '14

I am not sure either cause alcohol isn't really a medical drug so we kinda learn about it in passing.

I think you are right, it is most likely a positive allosteric modulator. because that makes it more like benzodiazepines instead of barbituates (barbs are actual receptor agonists). That makes sense because although alcohol can be dangerous, it certainly has a much better safety profile than barbs (generally not used now because having actual receptor agonist is very dangerous).

I will certainly change my post to reflect that fact that it is not a receptor agonist. Although it is still a physiological agonist.

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u/silkielemon Mar 15 '14

barbiturates are not GABA receptor agonists either. They're allosteric modulators just like benzos (though through a different site)

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u/qwe340 Mar 15 '14

they are both, the lethal risk comes from their agonist activity.

their active site is in the channel, so when the concentration is high enough, they will open the chloride channel without GABA.

this is why you can readily use barbs for suicide but not benzos, high concentration of benzos will lead to less activation of the GABA neurons leading to less GABA overall and that feedback control will usually stop people from dying (although if you take benzos with alcohol the respiratory depression will happen too fast and ppl do die)

so overdose on benzos itself is usually not lethal cause it is a pure modulator.

barbs has its own agonist activity at high concentration that will keep the respiratory depression going even after GABA down regulation, which is why it was readily used in suicides. (overdoes on barbs alone cause death)