It's possible I guess. Certainly for many years I had moderate-to-severe generalized anxiety disorder (GAD), and GAD might be due to high NMDA or low GABA (NMDA excites neurons and GABA relaxes neurons).
But is is hard to increase the GABAergic system in a safe way. Benzodiazepines can do it, but have issues of tolerance and withdrawal.
Kava kava may be the best option: this increases the number of GABA binding sites over time.
My anxiety levels greatly increased after catching coxsackievirus B4. It's interesting that CVB4 might trigger an autoimmune attack on the enzyme GAD65, which synthesizes GABA for neurotransmission. I posted about this in this post.
It may be that the amitriptyline you take helps with rising GABA.
Did you ever try GABAergic drugs like Gabapentin or Pregabalin?
These drugs are used in restless legs syndrome, an hyperarousal state with low GABA and low dopamine, (And maybe high glutamate and low adenosine)
Any way, if I had low GABA, I would look into my iron status. Both non anemic iron deficiency and iron overload can produce lower GABA inhibition.
Restless legs syndrome (RLS) is a chronic neurological disorder that interferes with rest and sleep.
It has a wide spectrum of symptom severity, and treatment is started when symptoms become bothersome.
Dopamine agonists and calcium channel apha-2-delta antagonists (gabapentin, gabapentin enacarbil and pregabalin) are first-line treatments; calcium channel alpha-2-deltas are preferred over dopamine agonists because they give less augmentation, a condition with symptom onset earlier in the day and intensification of RLS symptoms.
Dopamine agonists can still be used as first-line therapy, but the dose should be kept as low as possible.
Iron supplements are started when the serum ferritin concentration is ≤75µg/L, or if the transferrin saturation is less than 20%. For severe or resistant RLS, a combined treatment approach can be effective. Augmentation can be very challenging to treat and lacks evidenced-based guidelines
Restless Legs Syndrome: clinical features, diagnosis and a practical approach to management (bmj.com)
Iron deficiency is closely associated with altered GABA metabolism and affective behavior.
While mutation in the hemochromatosis (HFE) gene disrupts iron homeostasis and promotes oxidative stress that increases the risk of neurodegeneration, it is largely unknown whether HFE mutation modifies GABAergic homeostasis and emotional behavior.
Taken together, our results suggest a putative role of HFE in regulating labile iron status in the brain, and mutation in H67D perturbs redox-methylation status, contributing to GABAergic dysfunction.—
Brain iron loading impairs DNA methylation and alters GABAergic function in mice - Ye - 2019 - The FASEB Journal - Wiley Online Library
In addition to the well-known dopaminergic involvement in RLS, previous studies pointed out that Brain Iron Deficiency brings also a hyperglutamatergic state that influences a dysfunctional cortico-striatal-thalamic-cortical circuit in genetically vulnerable individuals.
However, the enhancement of arousal mechanisms in RLS may also be explained by functional changes of the ascending arousal systems and by deficitary GABA-mediated inhibitory control.
Very recently, it was also suggested that BID induces a hypoadenosinergic state in RLS, thus possibly providing a link for a putative unified pathophysiological mechanism accounting for both hyperarousal and sensory-motor signs.
The neurophysiology of hyperarousal in restless legs syndrome: Hints for a role of glutamate/GABA - ScienceDirect
These preliminary results suggest that dipyridamole has significant therapeutic effects on both sensory and motor symptoms, as well as sleep. In addition, it provides evidence that hypoadenosinergic mechanisms play a central role in RLS.
Treatment of restless legs syndrome/Willis-Ekbom disease with the non-selective ENT1/ENT2 inhibitor dipyridamole: testing the adenosine hypothesis - ScienceDirect