It's possible that glutamate excitation increases GABA neurotransmission, but...

...this doesn't help in withdrawal (or may exacerbate it).

Furthermore, if increases in GABA neurotransmission do occur, it also makes sense that it would have no effect (again, if not exacerbating!) on receptors, since they are desensitized and dispersed along the cell surface.

This would further impede or altogether halt GABA re-coupling and ultimately healing.

Reduced efficacy of critical calcium transfer levels from glutamate stores to GABA ones - which are responsible for re-coupling - might be rendered ineffective or negligibly so. This could either help explain inability to also re-sensitize or not explain the dilemma of re-sensitivity at all.

Given the action of some nootropics, many of which interrupt the conversion of glutamate to GABA (ie. PPK, B6, etc.), it may be more clear why they're so helpful (reductions in GABA ligand (neurotransmitter) could trigger dependent up-regulation response).

It's clear that glutamate has complete endemic control of GABA functionality, so the etiology is likely complicated...

Still, I think the focus should be directed towards the GABA side.

Quick note...

In the case of coffee-based caffeine as a potential regeneration mechanism, it is thought that stimulation is conducted with little to no NMDA or calcium channel activity. This might mean that, a.) caffeine-mediated GABA antagonism without NMDA and calcium involvement could enable the desired end; or b.) caffeine-mediated GABA antagonism without NMDA and calcium involvement provides enough stress to 'unlock' receptors and re-sensitize; or c.) both.

In the case of ginkgo biloba, where GABA neurotransmitter genesis (mentioned above) is interrupted, along with some glutamate neurotransmitter reductions and reduced calcium channel intake, there may exist some similar effect as the caffeine proposal.

    In these cases and trials where coffee-based caffeine was employed and GABA regulation/restoration was seen very quickly, it would make some sense.

I'm convinced that the one thing that makes regeneration in withdrawal so hard is the vicious cycle played out in the body.

Chronic benzo dosing has created two primary things: deficiency and imbalance.

I realize both are inter-correlated, as deficiency leads to imbalance and vice versa, but bear with me...

My amateur research consistently brings me back to the GABA side of the equation.

...of course, I've completely left out altered genetic expression. 

FandF