Glycine as a neurotransmitter: Glycine is stored vesicularly in glycinergic neurons. It is released exocytotically after adequate stimulus. It acts via the ionotropic glycine receptor. An inhibitory postsynaptic potential (IPSP) occurs via the opening of ligand-gated chloride channels, which decreases the activity of the downstream neuron. At the NMDA receptor, on the other hand, it has a stimulatory effect at a specific glycine-binding site, in addition to the main agonist glutamate.
A down-regulation of the glycine effect is caused by strychnine, which blocks the binding site of the glycine receptor as an antagonist. Taurine , on the other hand, is an agonist of the glycine receptor. Tetanus toxin inhibits the release of glycine. Tetanus toxin, which has a proteolytic effect, selectively destroys a protein in the salivary vesicles of glycine and GABA that is important for exocytosis, thus blocking the release of the transmitters. The result is the characteristic spasms and convulsions(tetanus=tetanus).
Abnormal accumulation of glycine can lead to glycine encephalopathy.