GlycinevsMagnesium Glycinate

Glycine acts as an inhibitory neurotransmitter by binding to strychnine-sensitive glycine receptors (GlyR) in the brainstem, spinal cord, and retina, hyperpolarizing neurons via chloride influx. It also serves as a mandatory co-agonist at the glycine-binding site (NR1 subunit) of NMDA glutamate receptors — without glycine binding, NMDA receptors cannot open their ion channel even when glutamate is present. This dual role means glycine both calms neural activity (sleep, anti-anxiety via GlyR) and supports excitatory learning processes (NMDA-dependent LTP and memory consolidation). Glycine lowers core body temperature at night by promoting peripheral vasodilation through nitric oxide, which improves sleep onset. It is a precursor for glutathione synthesis and modulates the glycinergic system in the suprachiasmatic nucleus.

Magnesium is required for over 300 enzymatic reactions including neurotransmitter synthesis (tyrosine hydroxylase, tryptophan hydroxylase), energy production (ATPases, kinases, glycolytic enzymes), and DNA repair (PARP, DNA polymerases). In the brain, magnesium blocks NMDA receptors at the voltage-dependent Mg2+ binding site within the channel pore (GluN1/GluN2 subunits), preventing excessive calcium influx and excitotoxicity — Mg2+ is displaced only upon depolarization and glycine/glutamate binding. The glycine component activates inhibitory glycine receptors (GlyR alpha1/alpha2) in the brainstem and spinal cord, and serves as an obligatory co-agonist at the GluN1 glycine site of NMDA receptors. Glycine also modulates NMDA receptor function. Together, magnesium and glycine produce calming effects through complementary inhibitory mechanisms: reduced glutamatergic excitability and enhanced inhibitory neurotransmission.