P1.15. POST-STROKE SOMATOSENSORY DEFICITS ARE REFLECTED IN ALTERED ACTIVITY OF SPINAL WDR NEURONS
Joanna Bernacka1, Jakub Jurczyk3, Weronika Krzyżanowska4, Bartosz Pomierny3, Mateusz Kucharczyk1,2
1 Cancer Neurophysiology Group, Łukasiewicz Research Network - PORT Polish Center for Technology Development, ul. Stabłowicka 147, 54-066, Wroclaw, Poland
2 Wolfson Sensory, Pain and Regeneration Centre, King’s College London, SE1 1UL London, UK
3 Imaging Laboratory, Center for the Development of Therapies for Civilization and Age-Related Diseases, Jagiellonian University Medical College, Medyczna 9, 30-688 Kraków, Poland
4 Jagiellonian University Medical College, Department of Toxicological Biochemistry, Chair of Toxicology, Medyczna 9, 30-688 Kraków, Poland
INTRODUCTION: Ischemic stroke is one of the leading causes of long-term disability. While motor deficits are widely discussed, somatosensory disorders – affecting up to 80% of patients – are often neglected. These include dysfunction in tactile sensation, proprioception, and stereognosis, significantly impairing motor recovery. Despite their prevalence, mechanisms underlying post-stroke sensory deficiencies and their dynamics remain poorly explored. Wide dynamic range (WDR) neurons in the spinal cord may reflect broader top-down changes in sensory processing after stroke.
AIM(S): To explore how ischemic stroke affects spinal WDR neurons activity over time in response to various sensory stimuli.
METHOD(S): Stroke was induced in male Sprague-Dawley rats using the Middle Cerebral Artery Occlusion (MCAO) model. The von Frey and Hargreaves behavioral tests assessed mechanical and thermal sensitivity over time. Electrophysiological recordings of lumbar WDR neurons were performed at 24h and 7 days post-MCAO using mechanical, thermal, and electrical stimuli. Infarct volume was analyzed using TTC staining and LASCA imaging.
RESULTS: We observed post-MCAO significant infarction. Behaviorally, rats showed hypoesthesia at 24h, followed by hyperesthesia by day 21 for both thermal and mechanical stimuli. Electrophysiological data showed reduced WDR responses to Aβ fiber input at 24h and enhanced responses to Aδ fibers and mechanical stimuli by day 7. Temporal summation and post-discharge were elevated at 7 days, indicating central sensitization. Additionally, diffuse noxious inhibitory control (DNIC) was absent at 24h and partially recovered by day 7.
CONCLUSIONS: Ischemic stroke leads to time-dependent disturbances in somatosensory processing, evolving from hypoesthesia to hyperesthesia and allodynia. These are paralleled by dynamic changes in WDR neuron excitability and DNIC dysfunction, suggesting impaired descending modulation. The findings emphasize the importance of spinal mechanisms in post-stroke sensory deficits.
FINANCIAL SUPPORT: This study was funded by the National Science Center research grant, MINIATURA no. 2022/06/X/NZ5/01381 and SONATA no. 2022/47/D/NZ4/02676 both awarded to Mateusz W. Kucharczyk.