ArticlePain reports2026
Ventral intraspinal microstimulation alters neural population-level nociceptive activity in rats including after spinal cord injury.
Article in Pain reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Spinal cord injury (SCI) often results in movement impairments and neuropathic pain. Objectives: The purpose of this study was to determine whether intraspinal microstimulation (ISMS) intended to enhance voluntary movement after SCI modulates neural population-level spinal responsiveness to nociceptive sensory input. Methods: The study was conducted in vivo in 3 cohorts of rats: neurologically intact, chronic SCI without behavioral signs of neuropathic pain, and chronic SCI with neuropathic pain. Nociceptive sensory input was induced by pinches of the plantar surface of the hind paw before, during, and after low frequency (7 Hz), submotor threshold ISMS delivered within or near the motor pools of the L5 spinal segment. Neural population-level responsiveness to nociceptive input was recorded throughout the dorso-ventral extent of the L5 spinal segment using microelectrode arrays. Results: Before ISMS, pinch-evoked multiunit discharge rates did not vary between cohorts, although both SCI cohorts had twice as many pinch-responsive electrodes as the neurologically intact cohort. The percentage of electrodes modulated during ISMS did not differ between cohorts, although excitatory actions were preferential in the SCI cohorts. After ISMS, all cohorts exhibited ≥2X more electrodes with altered pinch responsiveness than during ISMS, with depressive actions predominant in the noninjured cohort. Conclusion: Doubling of the number of electrodes with altered pinch responsiveness after ISMS suggests that ISMS causes a lasting increase in the spatial spread of evoked sensory activity. That this change favored inhibition in 1 cohort is consistent with the possibility of ventral ISMS promoting broad inhibitory control of nociceptive activity.
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