The common view is that glycine serves as an inhibitory neurotransmitter at the level of the spinal cord while GABA is the primary inhibitory neurotransmitter in brain. Several lines of more recent evidence, however, indicates that glycine acts as an inhibitory transmitter also in brain. Glycine-mediated Cl^- fluxes have been demonstrated in cells and synaptic preparations from different parts of the brain of adult animals using electrophysiology and novel fluorescent indicators for Cl^-. Glycine receptor mRNA expression is widespread in brain and the structure of the brain glycine receptors is different compared to the spinal cord. Immunocytochemistry has also shown that the expression of the inhibitory glycine receptors changes during development. The brain glycine receptors changes during development. The brain glycine receptors may be different with respect to their lower sensitivity to strychnine and therefore no or little autoradiographic labelling is seen using [³H]-strychnine. Interestingly, ethanol potentiates the response to glycine in a similar manner to its effect on GABA-receptor mediated response. Nerve terminals containing glycine within synaptic vesicles have been demonstrated in brain using immunohistochemistry. Demonstration and cloning of Na⁺-dependent high affinity glycine transporters as well as the release of glycine from superfused hippocampal synaptosomes that has been reported to the both Ca²⁺-dependent (specific feature of transmitter) and Ca²⁺-independent further suggest that glycine may act as a neurotransmitter in brain.