Abstract

The two amino acids GABA and glycine mediate fast inhibitory neurotransmission in
different CNS areas and serve pivotal roles in the spinal sensory processing. Under
healthy conditions, they limit the excitability of spinal terminals of primary sensory nerve
fibers and of intrinsic dorsal horn neurons through pre- and postsynaptic mechanisms, and thereby
facilitate the spatial and temporal discrimination of sensory stimuli. Removal of fast inhibition not
only reduces the fidelity of normal sensory processing but also provokes symptoms very much
reminiscent of pathological and chronic pain syndromes. This review summarizes our knowledge of
the molecular bases of spinal inhibitory neurotransmission and its organization in dorsal horn
sensory circuits. Particular emphasis is placed on the role and mechanisms of spinal inhibitory
malfunction in inflammatory and neuropathic chronic pain syndromes.