From Wikipedia:
Piracetam's
mechanism of action, as with
racetams in general, is not fully understood. The drug influences neuronal and vascular functions and influences cognitive function without acting as a sedative or stimulant.
[9] Piracetam is a
positive allosteric modulator of the
AMPA receptor, although this action is very weak and its clinical effects may not necessarily be mediated by this action.
[27] It is hypothesized to act on ion channels or ion carriers, thus leading to increased neuron excitability.
[25] GABAbrain metabolism and GABA receptors are not affected by piracetam
[28]
Piracetam improves the function of the
neurotransmitter acetylcholine via
muscariniccholinergic (ACh)
receptors[
citation needed], which are implicated in
memory processes.
[29] Furthermore, piracetam may have an effect on
NMDA glutamatereceptors, which are involved with
learning and
memory processes. Piracetam is thought to increase cell membrane permeability.
[29][30] Piracetam may exert its global effect on brain neurotransmission via modulation of
ion channels (
i.e., Na+, K+).
[25] It has been found to increase oxygen consumption in the brain, apparently in connection to
ATP metabolism, and increases the activity of
adenylate kinase in rat brains.
[31][32] Piracetam, while in the brain, appears to increase the synthesis of
cytochrome b5,
[33] which is a part of the
electron transport mechanism in
mitochondria. But in the brain, it also increases the permeability of some intermediates of the
Krebs cyclethrough the mitochondrial outer membrane.
[31]
Piracetam inhibits
N-type calcium channels. The concentration of piracetam achieved in
central nervous system after a typical dose of 1200 mg (about 100 μM)
[34] is much higher than the concentration necessary to inhibit
N-type calcium channels (
IC50 of piracetam in rat neurons was 3 μM).
[35]
