Peripheral inflammation facilitates A beta fiber-mediated synaptic input to the substantia gelatinosa of the adult rat spinal cord

Whole-cell patch-clamp recordings were made from substantia gelatinosa (SG) neurons in thick adult rat transverse spinal cord slices with attached dor sal roots to study changes in fast synaptic transmission induced by periphe ral inflammation. In slices from naive rats, primary afferent stimulation a t Ap fiber intensity elicited potysynaptic EPSCs in only 14 of 57 (25%) SG neurons. In contrast, A beta fiber stimulation evoked polysynaptic EPSCs in 39 of 62 (63%) SG neurons recorded in slices from rats inflamed by an intr aplantar injection of complete Freund's adjuvant (CFA) 48 hr earlier (p < 0 .001). Although the peripheral inflammation had no significant effect on th e threshold and conduction velocities of A beta, A delta, and C fibers reco rded in dorsal roots, the mean threshold intensity for eliciting EPSCs was significantly lower in cells recorded from rats with inflammation (naive: 3 3.2 +/- 15.1 mu A, n = 57; inflamed: 22.8 +/- 11.3 mu A, n = 62, p < 0.001) , and the mean latency of EPSCs elicited by AP fiber stimulation in CFA-tre ated rats was significantly shorter than that recorded from naive rats (3.3 +/- 1.3 msec, n = 36 vs 6.0 +/- 3.5 msec, n = 12; p = 0.010). AP fiber sti mulation evoked polysynaptic IPSCs in 4 of 25 (16%) cells recorded from nai ve rat preparations and 14 of 26 (54%) SG neurons from CFA-treated rats (p < 0.001). The mean threshold intensity for IPSCs was also significantly low er in CFA-treated rats (naive: 32.5 +/- 15.7 mu A, n = 25; inflamed: 21.9 /- 9.9 mu A, n = 26, p = 0.013). The facilitation of AP fiber-mediated inpu t into the substantia gelatinosa after peripheral inflammation may contribu te to altered sensory processing.