Plastic changes in sensory inputs to rat substantia gelatinosa neurons following peripheral inflammation

Although hyperalgesia elicited by inflammation has been shown to be partly due to central sensitization, the cellular mechanisms are not clear at the moment. The present study was designed to address this issue using the blin d whole-cell patch-clamp technique; glutamatergic primary-afferent inputs t o substantia gelatinosa (SG) neurons were compared between spinal cord slic es of naive rats and rats inflamed by an intraplantar injection of complete Freund's adjuvant. In naive rats, a large number of SG neurons examined re ceived monosynaptic A delta- (69% of 41 neurons innervated by A fibers) and /or polysynaptic C- (94% of 36 neurons innervated by C fibers) afferent inp uts, and only a few neurons received monosynaptic A beta inputs (7%), In ad dition, when examined in neurons which have both of the A- and C-afferent i nputs, A afferent-evoked excitatory postsynaptic currents (EPSCs) were larg er in amplitude than C afferent-induced ones; a ratio (A/C ratio) of the fo rmer to latter amplitude was 1.8 +/- 0.1 (n = 36). In inflamed rats, a chan ge in the synaptic responses was observed: (1) SG neurons receiving monosyn aptic A delta-afferent inputs decreased in number (to 20% of 30 neurons tes ted, innervated by A fibers), whereas those having monosynaptic A beta-affe rent inputs increased to 33%, and (2) the A/C ratio decreased to 0.7 +/- 0. 1 (n = 33). These results suggest that after inflammation, a substantial nu mber of A beta-afferents sprout into the SG from their original location (l aminae m-V) and that sensory information that used to be conveyed directly to the SG through A delta afferents is transmitted there indirectly through interneurons. These reorganizations of sensory pathway may contribute, at least in part, to underlying mechanisms for the development of hyperalgesia due to inflammation. (C) 1999 International Association for the Study of P ain. Published by Elsevier Science B.V.