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.
we say that anandamide may be more tonic and 2ag might be more phasic and like brought online when needed but doesn't do a lot there is some evidence that 2ag may also have a role to regulate some circuits under kind of resting conditions as well
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2 AG is like the pinch hitter who gets brought in to do the heavy lifting and so 2 AG during a situation like let's say something like even like a seizure as an extreme example where you have a huge amount of neural activity those neurons that are getting heavily activated during you know massive amounts of neural activity start dumping out huge amounts of 2ag and that acts as the okay we really need to turn off this circuit very quickly in this situation and in most of these forms of like synaptic plasticity like I was saying earlier where you need to either strengthen or weaken a synapse in response to a change in the environment or in response to an experience or something that's going on most of that is driven by 2ag signaling
so most people who study like neurophysiology and like record activity in neurons and look at endoc canabo they're almost entirely talking about 2ag when they play with stuff
anandamide might be more of aonic molecule and what I mean by that is we'll say it's like a stage Setter so like an emide might just be kind of made by neurons on an ongoing basis and just released and its job may be to kind of keep the steady state of a brain circuit in a desired range so that under resting conditions it's not too active or too quiet your thermostat analogy is perfectly
the end of the day do the same thing they're regulating neurotransmitter release um through retrograde signal but what stimulation brings them online or what drives their activity May differentiate and we don't really understand all the details behind that outside of the fact that we very clearly know 2ag is activity dependent so as that neuron becomes more active it's going to make 2ag to regulate its inputs