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d-serine and huperzine-a

Why would dosing both be pointless?

Huperzine A deals with Acetylcholine and D-Serine activates the NMDA receptor.

If Racetams are intrinsic with D-Serine, you should be fine.
 
In rats (scaled for HED), it takes about 33 mg of huperzine to restrict NMDA-induced excitotoxicty (in the epilepsy model). Kinetically (in humans), 1 mg of huperzine achieves a Cmax of 0.034 micromoles, whereas (in vitro) the NMDA IC50 of huperzine is 45.4 micromoles.

And although the data is fairly clear that no meaningful level of NMDA inhibition will occur with low-to-normal dosed huperzine, there are better alternatives available (i.e. galantamine).
 
lronFist said:
Huperzine, nor the mechanisms involved with its usage, has nothing to do with focus, and it certainly wouldn't be an acute event.
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Will anything involving ACh or NMDA confer the sensation of focus? I always thought the sensation of focus was derived from the reticular activating system, which stimulants would influence.
 
domore said:
Will anything involving ACh or NMDA confer the sensation of focus? I always thought the sensation of focus was derived from the reticular activating system, which stimulants would influence.
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Ach plays a very limited role in augmenting/coordinating certain projections of the RAS.
 
lronFist said:
Ach plays a very limited role in augmenting/coordinating certain projections of the RAS.
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Good deal.

In respect to memory, NMDA agonists play an role in LTP and short-term memory, correct?---D-Serine, DAA, Sarcosine; your preference on a study stack: ALCAR, CDP-Choline, PhenylP, ...?
 
domore said:
Good deal.

In respect to memory, NMDA agonists play an role in LTP and short-term memory, correct?---D-Serine, DAA, Sarcosine; your preference on a study stack: ALCAR, CDP-Choline, PhenylP, ...?
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Ach and glutamate are intimately tied to encoding memory, yes.

For an acute study stack, I would opt for caffeine, galantamine, and maybe methylphenidate. Long term: DHA, galantamine, ALCAR, CDP-Choline/Alpha-GPC/adequate choline source. I wouldn't necessary reach for a racetam unless I was aged, or pathological.
 
lronFist said:
Ach and glutamate are intimately tied to encoding memory, yes.

For an acute study stack, I would opt for caffeine, galantamine, and maybe methylphenidate. Long term: DHA, galantamine, ALCAR, CDP-Choline/Alpha-GPC/adequate choline source. I wouldn't necessary reach for a racetam unless I was aged, or pathological.
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Galantamine is an agonist on ionotropic nicotinic receptors, too? Will you explain the benefit of the activation of the nAChRs (triggered by binding of ACh)?

While I'm looking to employ a study stack for my professional exams, methylphenidate will make me pop USAW/USADA drug tests for my competitions. How about a substitute?

I've read your racetam article. I'm looking forward to part two.
 
domore said:
Galantamine is an agonist on ionotropic nicotinic receptors, too? Will you explain the benefit of the activation of the nAChRs (triggered by binding of ACh)?

While I'm looking to employ a study stack for my professional exams, methylphenidate will make me pop USAW/USADA drug tests for my competitions. How about a substitute?

I've read your racetam article. I'm looking forward to part two.
Click to expand...

In the context of memory, nAchR's help to activate glutaminergic neurons in the hippocampus by amplifying the strength of post-synaptic signaling (meaning, the nidus for continued action potential is lessened).

If you can't utilize MPH, then I would just use caffeine.
 
lronFist said:
In the context of memory, nAchR's help to activate glutaminergic neurons in the hippocampus by amplifying the strength of post-synaptic signaling (meaning, the nidus for continued action potential is lessened).

If you can't utilize MPH, then I would just use caffeine.
Click to expand...

I appreciate the help. I'm glad you're posting; I love learning from your posts.
 
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