Potential New Treatment for Reversing Benzo Brain Damage (PAWS)

I have become kindled through multiple benzos binges and severe cold turkery withdrawals from GABAergics. 10 days ago I drank 2 glasses of wine and was unable to sleep for 2 days, and so far have had 2-4 hours of sleep a night with a BPM of 90 - 110. Previously I had binged 1 month ago, and since then I was waking up 1-2 hours too early with no improvement in symptoms over the course of 30 days.

Each abrupt GABA withdrawal kindles and permanently sensitizes the glutamate system, especially AMPA receptors. This process can also be caused by things like seizures and even manic episodes in bipolar. Along with changes in GABA receptors, this senstisation is a leading cause of PAWS (post acute withdrawal symptoms) in gabaergic cessation.

I came across some studies that showed that sarcosine reverses glutamergic sensitisation caused by seizure kindling and excess glutamate from schizophrenia. Should I give it a try? Could sarcosine worsen my symptoms - apparently it increases glutamate in mGluR5 knockout mice? I know very little about neurology and don't want to cause any further damage.

Studies:

" Together, these findings suggest that sarcosine has unprecedented disease-modifying properties in a kindling model of epileptogenesis in rats, which was associated with altered hippocampal DNA methylation. "

- https://www.frontiersin.org/articles/10.3389/fnmol.2020.00097/full

" This is the first study showing that a pharmacological intervention in schizophrenia, particularly augmentation of the antypsychotic treatment with sarcosine, may reverse the pathological increase in glutamatergic transmission in the hippocampus. "

- https://www.sciencedirect.com/science/article/abs/pii/S0304394015301099

Any thoughts on it? It's an OTC amino acid that is naturally produced by the body, so it should be safe. I have already tried it several months ago for depression (before any of my kindling problems) with no side effects.

It would appear that both AMPA and NDMA receptors play a role in sedative rebound effect:

These data indicate that NMDA-dependent mechanisms contribute to the development of tolerance to diazepam and to the expression of signs of dependence in mice after termination of long-term treatment with diazepam. Nevertheless, the non-NMDA-mediated silent phase is essential for triggering the symptoms. Therefore, AMPA antagonists may offer a therapeutic approach for preventing dependence on benzodiazepines that is an alternative to NMDA antagonism.

In the first three days post-cessation AMPA, in the following three weeks NDMA. So it would appear that playing around with glutamate antagonists cannot be done in straithforward manner, but rather requires a very specific timing i.e. block AMPA for three days, then block NDMA for three weeks.

I've found something that may normalize AMPA receptors. What do you think?

http://www.benzobuddies.org/forum/index.php?topic=245158.0

Also I've found one other person who's used sarcosine on this forum, who said that it helped his hypertension a lot.