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Comment · Sat, September 7, 2013 · Ceretropic

Is it necessary to maintain a piracetam blood serum level?

Original post in this thread

Damderiam · 20 points

With a half life of 4-5 hours it would require measuring and taking exact doses 3-4 times a day, and that's just not feasible all the time. However, there are plenty of medicines that continue to act, indirectly, after they've been eliminated. Am I getting any effect at all by taking it prior to bedtime, or would a morning dose be necessary as well? Since we don't know exactly how piracetam works I'll have to go by anecdotes and experimental evidence, but it's better than winging it. I figure it may, for example, increase the efficiency of sleep, or have lingering effects.

What they were answering

AgentLiquid · 1 points

I wholeheartedly agree with you - there's so much nonsense out there that appears to be legit, but isn't. Oh well, that's research for you, gotta filter out all the nonsense.

Ok, so you're thinking that the racetams increase production of catecholamines in the adrenal glands? Do you think the effect is direct (racetam interacts with the adrenal gland tissue directly) or indirect (racetam promotes release of ACTH by the pituitary, which then stimulates the adrenal glands)?

Something else to keep in mind is that perhaps oxiracetam has a more potent effect per weight. Maybe the extra hydroxyl group facilitates better neuronal membrane fluidity or something, who knows.

u/MisterYouAreSoDumb · Ceretropic

Probably indirectly. I got some more interesting studies.

https://hotfile.com/dl/243787443/e59c454/Blockade_of_the_nootropic_action_of_piracetam-like_nootropics_by_adrenalectomy-_an_effect_of_dosage.pdf.html

>It is equally possible
that the action of no otropics may occur through,
or be blocked by, modulation of the release of
adrenal products, e.g. aldosterone, corticosterone
or adrenaline, or of pituitary hormones (ACTH).
The steroids might be necessary for transport of
the no otropics through membranes, or vice versa.
Plastic processes in the brain could also account
for the loss of effect: the animals have to be
allowed a 5-day recovery period after adrenalectomy, and during that time plastic processes,
e.g. changes in receptor density or sensitivity,
presumably take place in the brain.

https://hotfile.com/dl/243787663/f6bcbdc/Involvement_of_a_steroidal_component_in_the_mechanism_of_action_of_piracetam-like_nootropics.pdf.html

>Pretreatment with aminoglutethimide completely blocked the effects of the 4 nootropics.
Whereas the retention performance of the mice pretrea-
ted with NaCl was distinctly improved by the nootropics,
no such effect was seen in those pretreated with 100
mg/kg orally of aminoglutethimide.

Pretreatment with the aldosterone antagonist epoxymexrenone also rendered all 4 nootropics inactive.

> Piracetam-like nootropics may modulate effects of
steroids on memory. Corticosterone, cortisol, dexamethasone, and dehydroepiandrosterone have already been
found to have positive effects on animal memory and there are dementia-like states in man that
can benefit from treatment with steroids.

https://hotfile.com/dl/243788991/e7c5b46/Aldosterone_receptors_are_involved_in_the_mediation_of_the_memory-enhancing_effects_of_piracetam.pdf.html

>The results obtained after aidosterone substitution
were very similar to those produced by corticosterone substitution: aldosterone substitution likewise restored
the effect of piracetam abolished by adrenalectomy, i.e.
in the aldosterone-substituted animals, the retention
performance of those given piracetam was significantly
better than that of the saline-treated controls (like that of
normal animals).

>The observations m a d e in Experiment were clearly
confirmed: corticosterone substitution (3/~g/ml drinking
fluid) restores the memory-enhancing effect of piracetam
after adrenalectomy; the effect was even m o r e distinct
than in Experiment. If the aldosterone receptors are
blocked with epoxymexrenon, however, the effect of
piracetam cannot be restored by corticosterone. It may
therefore be assumed that the restorative effect of
corticosterone is very probably mediated by activation of
the mineralocorticoid (Type I) receptors.

So it would seem that their effects are mediated by aldosterone receptor activation, most likely by some indirect mechanism.

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