Plastic changes in sensory inputs to dorsal horn neurons following peripheral inflammation

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Whole cell patch clamp recordings were made from dorsal horn neurons in thick adult rat transverse spinal cord slices with attached dorsal roots to study changes in synaptic transmission induced by peripheral inflammation and action of PGE2 on dorsal horn neurons. In naive rats, primary afferent stimulation at Aβfiber intensity elicited polysynaptic excitatory postsynaptic currents (EPSCs) in only 14 of 57 (25%) lamina II (SG) neurons. In contrast, Aβ fiber stimulation evoked polysynaptic EPSCs in 39 of 62(63%) SG neurons recorded from rats inflamed by an intraplantar injection of complete Freund's adjuvant (CFA) 48h earlier. The mean threshold intensity for eliciting EPSCs was significantly lower in cells recorded from rats with inflammation (naive : 33.2±15.1μA, n=57 ; inflamed : 22.8±11.3μA, n=62) and the mean latency of EPSCs elicited by Aβfiber stimulation in CFA-treated rats was significantly shorter than that recorded from naive rats (3.3±1.8 ms n=36 vs. 6.0±3.5 ms n=12). Bath applied PGE2 (1-20 μM) induced an inward current or membrane depolarization in the majority of deep dorsal horn neurons (laminae III-VI ; 83 of 139 cells), but only in a minority of lamina II neurons (6 of 53 cells). PGE2-induced inward currents were unaffected by perfusion with a Ca^<2+> free / high Mg^<2+> (5 mM) solution, and inhibited by flufenamic acid (50-200 μM), a nonselective cation channel blocker. The facilitation of Aβfiber-mediated input into the SG follwing peripheral inflammation may contribute to altered sensory processing. PGE2 may contribute to peripheral inflammation-induced dorsal horn neuron hyperexcitability by directly depolarizing a subset of dorsal horn neurons.