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A chronic compression of the DRG (CCD) produces cutaneous hyperalgesia and an enhanced excitability of neuronal somata in the compressed ganglion. The hyperpolarization-activated current (Ih), present in the somata and axons of DRG neurons, acts to induce a depolarization after a hyperpolarizing event and, if upregulated after CCD, may contribute to enhanced neuronal excitability. Whole-cell patch-clamp recordings were obtained from acutely dissociated, retrogradely labeled, cutaneous, adult rat DRG neurons of medium size. Neurons were dissociated from L4 and L5 control DRGs or DRGs that had each been compressed for 5–7 d by L-shaped rods inserted into the intervertebral foramina. Ih, consisting of a slowly activating inward current during a step hyperpolarization, was recorded from every labeled, medium-sized neuron and was blocked by 1 mm cesium or 15 μmZD7288. Compared with control, CCD increased the current density and rate of activation significantly without changing its reversal potential, voltage dependence of activation, or rate of deactivation. Because Ih activation provides a depolarizing current to the neuron, thus enhancing neuronal excitability, our results are consistent with the hypothesis thatIh contributes to hyperalgesia after CCD-induced nerve injury.

Upregulation of the Hyperpolarization-Activated Cation Current after Chronic Compression of the Dorsal Root Ganglion