Mercury + GABAB → Mg2+ Deficit → Ca2+ Overload → Stiffness
Biochemical Pathway ReportHeavy metal accumulation from Mercury (Hg) begins a destructive cascade in the central nervous system by targeting high-affinity sulfhydryl groups.
Chronic exposure selectively degrades and alters the expression of structural GABAB receptors, crippling the brain's baseline inhibitory control networks.
The failure of inhibitory signaling disrupts normal ion homeostasis, leading to a profound intracellular Magnesium (Mg2+) deficit inside the cellular matrix.
Without sufficient magnesium to block the gates, NMDA channels remain open, prompting a massive, toxic Calcium (Ca2+) overload.
Continuous calcium influx forces relentless actin-myosin cross-bridging, causing permanent muscle tone elevation, stiffness, and failure to relax.
Therapeutic application of Glycine serves to stimulate alternate inhibitory paths, helping to re-establish polarization and damp down systemic hyperexcitability.