Spinal nociceptive reflexes are sensitized in the monosodium iodoacetate model of osteoarthritis pain in the rat.

OBJECTIVE

Evidence suggests that osteoarthritis (OA) is associated with altered central pain processing. We assessed the effects of experimentally induced OA on the excitability of spinal nociceptive withdrawal reflexes (NWRs), and their supraspinal control in a preclinical OA model.

DESIGN

Experimental OA was induced in rats with knee injection of monosodium iodoacetate (MIA) and pain behaviour was assessed. 14/28 days post-MIA or saline injection, rats were anaesthetised for spinal NWR recording from tibialis anterior (TA) and biceps femoris (BF) hind limb muscles during plantar hind paw stimulation. Thresholds, receptive field sizes and wind up (incremental increase to repetitive stimulation) were measured in intact (d14/28) and spinalised (severed spinal cord; d28) MIA- and saline-injected rats.

RESULTS

MIA reduced BF mechanical thresholds at day 28. Spinalisation of MIA rats did not prevent this hyperexcitability, and failed to produce the reduction in reflex receptive field (RRF) size observed in saline rats. These data indicate that MIA induces a hyperexcitability of BF NWR circuits that is maintained at the spinal level. In contrast, MIA appeared to have no effect on NWRs evoked by mechanical stimuli in the ankle flexor TA in intact rats, however spinalisation revealed hyperexcitability. Thus, 28 days following MIA-treatment, descending supraspinal inhibition normalised TA NWRs and was only overcome following repetitive noxious stimulation during wind up.

CONCLUSIONS

We demonstrate that spinal nociceptive reflex pathways are sensitized following the development of OA, suggesting the presence of central sensitization. Further, our data reflect OA-induced alterations in the descending control of reflex responses. Our findings contribute to a mechanism-based understanding of OA pain.