Peripheral Inflammation Facilitates Aβ Fiber-Mediated Synaptic Input to the Substantia Gelatinosa of the Adult Rat Spinal Cord

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Abstract
Whole-cell patch-clamp recordings were made from substantia gelatinosa (SG) neurons in thick adult rat transverse spinal cord slices with attached dorsal roots to study changes in fast synaptic transmission induced by peripheral inflammation. In slices from naive rats, primary afferent stimulation at Aβ fiber intensity elicited polysynaptic EPSCs in only 14 of 57 (25%) SG neurons. In contrast, Aβ fiber stimulation evoked polysynaptic EPSCs in 39 of 62 (63%) SG neurons recorded in slices from rats inflamed by an intraplantar injection of complete Freund’s adjuvant (CFA) 48 hr earlier (p< 0.001). Although the peripheral inflammation had no significant effect on the threshold and conduction velocities of Aβ, Aδ, and C fibers recorded in dorsal roots, the mean threshold intensity for eliciting EPSCs was significantly lower in cells recorded from rats with inflammation (naive: 33.2 ± 15.1 μA,n= 57; inflamed: 22.8 ± 11.3 μA,n= 62,p< 0.001), and the mean latency of EPSCs elicited by Aβ fiber stimulation in CFA-treated rats was significantly shorter than that recorded from naive rats (3.3 ± 1.8 msec,n= 36 vs 6.0 ± 3.5 msec,n= 12;p= 0.010). Aβ fiber stimulation evoked polysynaptic IPSCs in 4 of 25 (16%) cells recorded from naive 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 lower in CFA-treated rats (naive: 32.5 ± 15.7 μA,n= 25; inflamed: 21.9 ± 9.9 μA,n= 26,p= 0.013). The facilitation of Aβ fiber-mediated input into the substantia gelatinosa after peripheral inflammation may contribute to altered sensory processing.