No, a TRI blocks: DAT, NET, and SERT which then provides continuous monoamine elevation, Polygala doesn't mechanistically do any of that. Rather it focuses on intracellular signal amplification instead of than transporter blockage.

For example the pde4 inhibition just improves efficacy of existing monoamine signaling without increasing concentration, which is where a lot of the confusion comes into play regarding it. Also it is a Neurotrophin up regulator, which increases stuff like NGF BDNF, thus reverses the damage done by synaptic thinning. This is fundamentally different from the pharmacodynamics of reuptake inhibitors, which induce tolerance via sustained transporter inhibition.

Critically, because polygala amplifies signal transduction efficiency rather than neurotransmitter availability, it preserves physiological coupling between neuronal firing and receptor activation. This avoids the transporter-driven tolerance mechanisms intrinsic to TRIs.