NoopeptvsPramiracetam

Noopept modulates AMPA and NMDA receptors similarly to racetams through positive allosteric modulation. Its key distinguishing feature is upregulation of BDNF (brain-derived neurotrophic factor) and NGF (nerve growth factor) via activation of TrkB and TrkA receptor signaling cascades — these neurotrophins are essential for neuronal growth, survival, dendritic arborization, and synaptic plasticity. Noopept inhibits glutamate-induced excitotoxicity by reducing calcium influx through NMDA receptors and modulating the NR2B subunit. It activates the PI3K/Akt and MAPK/ERK pathways downstream of neurotrophin receptors. The active metabolite cycloprolylglycine (a cyclic dipeptide) has endogenous nootropic activity, potentially acting as a trace amine-associated receptor ligand. Neuroprotection is further mediated through antioxidant effects and mitochondrial stabilization.

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.