Alcohol and GABA

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drobgyn32

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Withdrawal, aka increased excitatory, why would there by MORE gaba stimulation, aka more inhibitory?

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GABA smoothes out body movement and alcohol inhibits the GABA receptors. After sobering up, the body is trying to compensate for the inhibition by increasing GABA levels, but now overstimulation of the receptors makes movements all herky-jerky.

From the q-stem: let "uncontrolled electrical activity" lead you to (C) increased action potentials.
 
GABA smoothes out body movement and alcohol inhibits the GABA receptors. After sobering up, the body is trying to compensate for the inhibition by increasing GABA levels, but now overstimulation of the receptors makes movements all herky-jerky.

From the q-stem: let "uncontrolled electrical activity" lead you to (C) increased action potentials.

The passage said that alcohol INCREASES the inhibitory activity of GABA. Hence, it is a depressant.
 
You have already answered the question yourself. The passage told you that alcohol increases GABA inhibitors' activity. Abrupt cessation will not reverse the effect: GABA receptors are still more reactive than they normal are.

Of all the answer choices, only C correctly describes this phenomena.

Now, why it leads to seizures is something you should explore for yourself ;)
 
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Now I think I am confused! @wizzed101 can you follow my train of thought?

Alcohol is a GABA-receptor agonist. It depolarizes the membrane, calming my body down so I feel chilled out when I'm getting crunk. How does the withdrawal part work? Are the more APs fired after the alcohol is cleared away? The internets is telling me that the GABA receptors get desensitized and NMDA receptors get more sensitive, but this would mean less GABA APs during withdrawal.
 
I do not know how exactly alcohol stimulates GABA receptors, but that is immaterial. The question stem stated that the patient in question was an alcoholic. This person had been exposed to such effect for a long time. Withdrawals are result of the nervous system trying to maintain homeostasis under this effect. The real question is how the brain reacted to alcohol.

We are told that alcohol increases the effect of GABA, so in order to counter this effect the brain has a couple of options: it can decrease the amount of GABA produced, or it can decrease the number of the now more sensitive GABA receptors. We don't know which, but as you can see, the end result is the same: without alcohol the effect of GABA is diminished. The lack of inhibition on neurons leads to seizure.
 
Alcohol acts its effects on GABA receptors since it's a GABA agonist and works as a depressant. Prolonged exposure to alcohol causes the body to experience a continuous inhibitory stimuli. As a result, the body knows it must adapt so it must return to homeostasis. Therefore, since the rate of alcohol consumption stays the same, neuronal cells will then internalize GABA receptors to minimize the effect of alcohol. The internalization of GABA receptors results in a tolerance which is why you then need more alcohol to elicit the same neuronal response. During withdrawal, the amount of alcohol consumed is completely extinguished, yet you still have a decreased amount of GABA receptors. As a result, since GABA is an inhibitory neurotransmitter, the same amount of GABA that was used to inhibit action potentials prior to alcohol consumption won't do the job well enough. A lack of inhibition will then cause more action potentials being fired, thus resulting in convulsions (Answer C).
 
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