Sustained peripheral nociceptive input disrupts interstimulus-interval-dependent sensory gating in the rat primary somatosensory cortex

Sensory gating is processed in thalamocortical pathways and depends significantly on the interstimulus interval. Somatosensory symptoms and temporal discrimination disturbances are associated with nociceptive conditions. We aimed to investigate the effects of capsaicin application on sensory gating. Paired pulse somatosensory stimuli with a wide range of interstimulus intervals (ISI) (35, 50, 80, 140, and 500 milliseconds) were applied to the median nerve, and evoked potentials were recorded from the primary somatosensory cortex in rats. We analyzed the latency, duration, amplitude, and ratio of the first (S1) and second (S2) responses, as well as early and late high-frequency oscillations (HFOs), at 60 and 120 minutes after capsaicin injection. Compared to the vehicle, capsaicin administration increased the S1 amplitude and area under the curve and decreased the S2/S1 amplitude ratio during the 2 hours of recordings. Both early and late components of S1 responses were significantly increased in the 50–150 Hz domain. The early component of the area under S1 increased prominently in the 400–800 Hz band. Observed effects of capsaicin appeared to be independent of interstimulus interval. We propose that capsaicin-induced sustained nociceptive input has modified the response gain, combined with the loss of the normal ISI-dependent recovery function. Capsaicin exerted a disproportionate effect on S1 responses, suggesting an action on the early processing of sensory inputs. Capsaicin administration noticeably altered the HFO profile of the initial response (S1) to electrical stimulation, most apparent in the 50–150 Hz domain. We could not clearly detect a significant contribution of ISI values to capsaicin’s effects on sensory processing regulation.