Inhibitory amino acids

The Gamma-amino butyrate (GABA) and glycine are the main inhibitory amino acids in the CNS with glycine containing higher abundance in brainstem and spinal cord than the forebrain. Many pathways incuded in motor control are GABAergic, as most of the interneurons in both cerebral and cerebellar cortices, and the Purkinje cells which provide the whole output of the cerebellar cortex which is shown in table below:

The GABA is synthesized from glutamate by glutamic acid decarboxylase (GAD), an enzyme virtually limited to GABAergic neurons. After release it is taken up by the transporters into both glia and neurons. It is catabolized to succinic the semi-aldehyde by mitochondrial enzyme GABA transaminase as shown in figure below.

Figure: GABA shunt. GAD=glutamic acid decarboxylase; glu, glutamate; GABA-T, GABA=transaminase; gln=glutamine. 

The GABA acts on GABAA receptors which are ligand-gated chloride channels and GABAB receptors which are GPCRs. Naturally, responses of these two classes of receptor can be discriminated by the GABAA antagonist bicuculline and the GABAB agonist baclofen.

The Neurotransmitter glycine is synthesized from serine by mitochondrial serine transhydroxymethylase. The Glycine transporters eliminate it from the synapse. In the spinal cord the Renshaw cells state nAChR and are excited by collaterals of motor neurons. The Renshaw cells use glycine as a transmitter and reduce the motor neurons which excite them, among the others. This is an illustration of recurrent inhibition. It serves to dampen the result of motor neurons. The glycine receptors resemble the GABAA receptors and are a Cl- channel. It is blocked by strychnine. Furthermore tetanus toxin blocks glycine release. Both of these agents are convulsants as they eliminate Renshaw cell inhibition.