BromantanevsOxiracetam

Bromantane upregulates tyrosine hydroxylase (TH)—the rate-limiting enzyme in catecholamine synthesis—and aromatic L-amino acid decarboxylase (AADC), the enzymes responsible for converting L-tyrosine to L-DOPA and then to dopamine. This increases neuronal dopamine production capacity rather than depleting vesicular stores like traditional stimulants. The mechanism may involve modulation of transcription factors or enzyme phosphorylation. Bromantane also has anxiolytic properties through enhancement of GABAergic transmission, possibly via GABA-A receptor modulation or increased GABA synthesis. The combination of upregulated dopamine synthesis in mesolimbic and nigrostriatal pathways with GABAergic dampening of anxiety circuits produces sustained motivation, focus, and reduced mental fatigue without the jitteriness or crash typical of dopamine-releasing agents.

Oxiracetam enhances glutamatergic neurotransmission through positive allosteric modulation of AMPA receptors, increasing the amplitude and duration of excitatory postsynaptic potentials. It increases the release of excitatory neurotransmitters glutamate and D-aspartic acid from hippocampal presynaptic terminals, acting as a glutamate analog. Oxiracetam stimulates protein kinase C (PKC) isoforms, particularly PKC-α and PKC-γ, which phosphorylate substrates involved in memory consolidation, long-term potentiation (LTP), and synaptic plasticity. PKC activation enhances NMDA receptor function and AMPA receptor trafficking to the synapse. Its mild stimulatory effect derives from cholinergic system enhancement via increased acetylcholine release and nicotinic α7 receptor potentiation in the cortex.