AniracetamvsPramiracetam

Aniracetam is a positive allosteric modulator of AMPA receptors, binding to the allosteric site and slowing receptor desensitization, which prolongs excitatory postsynaptic currents and facilitates long-term potentiation. It also modulates group II metabotropic glutamate receptors (mGluR2/mGluR3), which regulate presynaptic glutamate release. Uniquely among racetams, aniracetam increases dopamine and serotonin release in the prefrontal cortex via modulation of monoamine transporter activity and vesicular release, contributing to its anxiolytic and mood-enhancing effects. It reduces GABAergic inhibition in the hippocampus through indirect modulation of GABA-A receptors, facilitating NMDA receptor activation and memory consolidation. The lipophilic phenylacetyl group enables rapid blood-brain barrier penetration.

Pramiracetam increases high-affinity choline uptake (HACU) in the hippocampus via potentiation of the choline transporter (CHT1), similar to but 15-30x more potent than coluracetam — dramatically increasing acetylcholine synthesis and release. It modulates AMPA glutamate receptors through positive allosteric modulation, enhancing excitatory neurotransmission. Pramiracetam increases neuronal nitric oxide synthase (nNOS) activity, elevating nitric oxide (NO) production and inducing cerebral vasodilation via cGMP-dependent pathways, thereby enhancing cerebral blood flow and oxygen delivery. The emotional flattening effect suggests significant modulation of prefrontal cortex activity, possibly through excessive cholinergic tone in limbic-prefrontal circuits or reduced dopaminergic/emotional salience signaling. It may also modulate sigma-1 receptor activity.