ebola?
Bluelight Crew
>>Selective α3 agonists are non sedating and non amnestic, purely anxiolytic (and anticonvulsant I think?)
>>
Really? What are some example agonists?
>>My main issue is with cognitive function. It seems that anti-cholinergics can be slightly cognitively deleterious and can make you physically sluggish (not as bad as potent GABA/sympathetic nervous system antagonists) during the day.>>
A long shot, but supplementing with lecithin (contains a precursor to acetylcholine) may help.
>>ps. I am still convinced that analysis via catecholamines isn't the correct explanation for memory issues. I believe it has more to do with large-scale neuro-endocrine changes.>>
Well...I'm guessing that there are multiple neuro-chemical "chains" that all support hippocampal activity, perhaps in different ways or domains. Thus, there'd be multiple ways to intervene with the formation of long-term memory.
This is bracketing aside the possibilities of wrecking STM (to hinder transfer and storage into and in LTM) or erasing LTM directly (not that we know how LTM works at all, really).
...
1. I wonder if its the case the the effect of psychedelics and stimulants on memory relates to their respective tendencies to dilate and constrict time...or perhaps their effects on anxiety.
2. Might a selective GABA antagonist improve the formation of new LTMs? Could it be made selective enough that it isn't anxiogenic?
ebola
>>
Really? What are some example agonists?
>>My main issue is with cognitive function. It seems that anti-cholinergics can be slightly cognitively deleterious and can make you physically sluggish (not as bad as potent GABA/sympathetic nervous system antagonists) during the day.>>
A long shot, but supplementing with lecithin (contains a precursor to acetylcholine) may help.
>>ps. I am still convinced that analysis via catecholamines isn't the correct explanation for memory issues. I believe it has more to do with large-scale neuro-endocrine changes.>>
Well...I'm guessing that there are multiple neuro-chemical "chains" that all support hippocampal activity, perhaps in different ways or domains. Thus, there'd be multiple ways to intervene with the formation of long-term memory.
This is bracketing aside the possibilities of wrecking STM (to hinder transfer and storage into and in LTM) or erasing LTM directly (not that we know how LTM works at all, really).
...
1. I wonder if its the case the the effect of psychedelics and stimulants on memory relates to their respective tendencies to dilate and constrict time...or perhaps their effects on anxiety.
2. Might a selective GABA antagonist improve the formation of new LTMs? Could it be made selective enough that it isn't anxiogenic?
ebola

