Stimulatory mechanism of high-dose pregabalin

[plumbus-nine]

While in low-moderate doses, as prescribed, pregabalin acts as an antiepileptic and anxiolytic by decreasing glutamate and increasing GABA indirectly by upregulating L-glu acid decarboxylase, it has a weird and interesting, reinforcing stimulatory effect when taken acute high (depending on individual tolerance) dosages, usually around 600mg or up to 3g for heavy tolerance. One proposed mechanism is by inhibiting reuptake of glutamate by interacting with GLT-1.

Is the a2d ca channel blockade even necessary for this sort of effect or does it only contribute to side effects? Could one come up with a more balanced substance which would not undergo pregabalin's astronomical tolerance curve?

Shouldn't very high doses then actually cause less withdrawal because rebound at GLT-1 would cause temporarily lowered glutamate, so aiding with recovery? Just avoid cold turkey.. ?

Are any (possibly plant based) modulators of these two enzymes known?