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Effect of Gamma-Aminobutyric Acid (GABA) and GABA Antagonist Drugs on ACTH Release
Makara GB, Stark E
Neuroendocrinology 1974;16:178–190 (DOI: 10.1159/000122564)

Abstract:
Corticotrophin (ACTH) release has been studied in rats given intraventricular gamma-aminobutyric acid (GABA) infusions or injections of picrotoxin and bicuculline. As an index of ACTH release the corticosterone level of blood or plasma was determined. GABA (1 M/liter), infused at a rate of 1 µl/min into the 3rd ventricle, inhibited the rise in plasma corticosterone normally produced by surgical trauma. 60 min after surgical trauma the rats given GABA infusions had lower blood corticosterone levels than the control rats given infusions of 1 M/liter of proline, 1 M/liter of glycine, or 0.15 M/liter of sodium chloride. Picrotoxin, an antagonist of GABA, is a potent stimulus of ACTH release. In sub-convulsive intraperitoneal doses it produced a significant rise in plasma corticosterone in conscious rats with complete hypothalamic deafferentation. Under pentobarbital anesthesia 12.5 µg of picrotoxin injected into the 3rd ventricle produced a small but significant rise in plasma corticosterone in rats with hypothalamic deafferentation. After intraventricular injections of bicuculline methiodide a significant rise in plasma corticosterone occurred in rats with hypothalamic deafferentation; the ACTH releasing effect of 2.5 µg of bicuculline methiodide was strongly inhibited by a simultaneous infusion of 0.15 M/liter of GABA. On the basis of this pharmacological evidence, we suggest that GABA may be an inhibitory neurotransmitter of hypothalamic interneurons and/or afferent pathways involved in the regulation of ACTH release.

GABA status is correlated with your zinc status. and that's only one of hundreds of important body functions in which zinc is involved.

zinc and GABA and the brain:
Release of glutamate and GABA in the hippocampus under zinc deficiency (2003)
http://onlinelibrary.wiley.com/doi/10.1 ... 0/abstract
Zinc homeostasis in the brain is affected by dietary zinc deficiency, and its alteration may cause brain dysfunctions... Gamma aminobutyric acid (GABA) concentration in the hippocampal extracellular fluid during stimulation with high K+ was increased in the control rats, but not in the zinc-deficient rats.

Impairment of GABAergic neurotransmitter system in the amygdala of young rats after 4-week zinc deprivation (2006)
http://www.sciencedirect.com/science/ar ... 8606002233
the basal GABA concentration in the amygdalar extracellular fluid was significantly lower in zinc-deficient rats and was not increased both in the control and zinc-deficient rats by stimulation with 100 mM KCl. These results suggest that GABAergic neurotransmitter system is critically impaired in the amygdala of young rats after 4-week zinc deprivation.

and as i've posted elsewhere, the WHO thinks about 30% of the population are zinc deficient, whether we live in developed or developing countries.

without adequate zinc, your liver cannot convert amino acid breakdown products to uric acid. all that happens is the ammonia byproduct from which uric acid is made (using zinc) goes up - people with low uric acid can have high levels of ammonia in their system.

obviously i don't think we're on the verge of coma but there must be a continuum of issues all the way up to fatal cases of hyperammonemia.