[1] The receptor can be activated by a range of simple amino acids including glycine, β-alanine and taurine, and can be selectively blocked by the high-affinity competitive antagonist strychnine.
[5] Nevertheless, some exceptions can occur in the central nervous system where the GlyR α1 subunit and gephyrin, its anchoring protein, are not found in dorsal root ganglion neurons despite the presence of GABAA receptors.
[8] Two years later, experiments showed that glycine had a hyperpolarizing effect on spinal motor neurons[9] due to increased chloride conductance through the receptor.
[11] All of these discoveries resulted in the conclusion that glycine is a primary inhibitory neurotransmitter of the spinal cord that works via its receptor.
[15] The α-subunits are also able to form functional homopentamers in heterologous expression systems in African clawed frog oocytes or mammalian cell lines, which are useful for studies of channel pharmacokinetics and pharmacodynamics.
[16] In mature adults, glycine is a inhibitory neurotransmitter found in the spinal cord and regions of the brain.
[18] This is because chloride has a more positive equilibrium potential in early stages of life due to the high expression of NKCC1.
The disorder is characterized by an exaggerated response to unexpected stimuli which is followed by a temporary but complete muscular rigidity often resulting in an unprotected fall.