Mechanisms of Pain Caused by Surgical Incision Investigated in a Rat Model. Vandermeulen et al.(page 1294)
Sensitization of the dorsal horn of the spinal cord via surgery (termed central sensitization) is not well-defined. Hypothesizing that a surgical incision would produce activation and enhanced responsiveness of single dorsal horn neurons, Vandermeulen et al. used a previously developed rat incisional pain model to study spontaneous and evoked activity from individual dorsal horn neurons in the lumbar spinal cord directly. After performing laminectomy in halothane-anesthetized rats, dorsal horn neurons from the lumbar enlargement were identified antidromically and characterized as low threshold, wide dynamic range, or high threshold based on their responses to brush and pinch of the animals’ paws. The receptive field for each neuron also was mapped. Then, an incision was made within the receptive field. Changes in background activity, punctate mechanical thresholds, receptive field size, and stimulus–response functions were recorded for up to 1 h after incision.
In all cells, incisions produced a strong response and an increase in background activity, which remained increased in 3 of 9 high-threshold neurons and 16 of 28 wide-dynamic-range neurons 1 h later. The mechanical responsiveness was enhanced in 10 of 27 wide-dynamic-range neurons and in 2 of 8 high-threshold cells after incision. Wide-dynamic-range neurons may be the most important for pain signaling, and the increased background activity in these dorsal horn neurons may signal pain at rest after surgery. The receptive field size also expanded beyond the initial area around the incision, indicating a mechanism for amplification of dorsal horn response via surgery.