The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
it's binding the very same type of receptors, CB1 receptors, in other brain structures, such as the amygdala and causing retrograde signaling back to the presynaptic neurons in the amygdala, but it's quieting the activation of those neurons
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
CB1 like THC will initially hit CB1 on kind of glutamatergic neurons and essentially the thought is this will reduce excitatory transmission and probably quiet down circuits and if we're talking about something like the amydala this is probably how it's reducing anxiety
if you delete CB1 only off of excitatory neurons you lose the anti-anxiety angiolytic effects of THC but you still have the you know panicky angiogenic effects of hos
as dosing starts to increase and you start to saturate the CB1 on the gabin neurons and turn off inhibition then the network effect is more of an amplification and that seems to result in the development of kind of an angiogenic uh pro- anxiety response
on glutamate neurons they're much more sensitive than they are in gabin neurons so there's probably a dose threshold