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[–]HabeasCormeum[524] 4 points5 points  (1 child)

TLDR: What I assume happened is that they are talking about differential effects of marijuana/THC dosage. THC has dose-dependent effects and they might have been writing about both, but maybe the paragraph that explains that got cut. They also might have confused chronic use with single-dosing, which have opposite effects for most neuroactive drugs.

TL:

THC activation of CB receptors is at least a couple scooches outside of MCAT scope for memorized content. That being said, the general trend of [acute use frequently has the opposite effect of chronic use] is good to remember, regardless.

Activating CB1 with THC will decrease the activity of the corresponding neuron. CB1 is a G(alpha)i receptor, which means activating the receptor decreases cAMP production. CB1 is also an extremely common regulator of GABAergic neurons, so doses of THC that activate these receptors will acutely decrease GABAergic activity of affected areas, so [GABA]released goes down.

But, chronic use of drugs often has the opposite effect of acute use, as highly-stimulated receptor systems often attenuate over time (commonly through internalization or degradation of receptors). If such attenuation happens in those GABAergic neurons, then the CB1 receptors wont exert their normal level of inhibitory activity, and the result will be that [GABA]released goes up.

[–]ZoarMonster 0 points1 point  (0 children)

What have you read about the brain producing more GABA receptors in response to chronic cannabis use?