Glycine is one of the most important inhibitory neurotransmitters in the sp
inal cord and the brainstem, and glycinergic synapses have a well-establish
ed role in the regulation of locomotor behavior. Research over the last 15
years has yielded new insights on glycine neurotransmission. Glycinergic sy
napses are now known not to be restricted to the spinal cord and the brains
tem. Presynaptic machinery for glycine release and uptake, the structure an
d function of postsynaptic receptors and the factors (both pre- and postsyn
aptic) which control the strength of glycinergic inhibition have been exten
sively studied. It is now established that glycinergic synapses can be exci
tatory in the immature brain and that some inhibitory synapses can coreleas
e gamma -aminobutyric acid (GABA) and glycine. Moreover, the presence of gl
ycine transporters on glial cells and the capacity of these cells to releas
e glycine suggest that glycine may also act as a neuromodulator. Extensive
molecular studies have revealed the presence of distinct subtypes of postsy
naptic glycine receptors with different functional properties. Mechanisms o
f glycine receptors aggregation at postsynaptic sites during development ar
e better understood and functional implications of variation in receptor nu
mber between postsynaptic sites are partly elucidated. Mutations of glycine
receptor subunits have been shown to underly some human locomotor disorder
s, including the startle disease. Clearly, recent work on glycine receptor
channels and the synapses at which they mediate inhibitory signalling in bo
th young and adult animals necessitates an update of our vision of glyciner
gic inhibitory transmission.