title: Bilateral hyperexcitability of thalamic VPL neurons following unilateral spinal injury in rats.
abstract: In the present study, we have examined whether spinal hemisection injury induces changes in the electrophysiological properties of thalamic ventral posteriorlateral (VPL) neurons in rats. Male Sprague-Dawley rats were subjected to unilateral spinal cord injury by transverse hemisection at the T13 spinal segment. Four weeks after the T13 spinal hemisection, the injured rats displayed robust allodynic behaviors on both sides of hindpaws compared to sham controls (P < 0.05). Extracellular recordings taken 4 weeks after the hemisection revealed that wide dynamic range (WDR) neurons had significantly increased spontaneous and brush-, pressure-, and pinch-evoked activities, respectively, on both sides of the thalamic VPL regions (P < 0.05). In contrast, low threshold (LT) neurons showed only an increase in the brush-evoked activity compared to sham controls (P < 0.05). However, afterdischarge activity in both types of neurons showed no changes. In addition, both sides of the thalamic VPL regions showed higher incidences of WDR neurons. In conclusion, our data demonstrate that spinal unilateral injury induces bilaterally increased evoked activity in thalamic VPL neurons.
authors.affiliation: Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555-1043, USA. ysgwak@utmb.edU
authors.forename: Young Seob
authors.initials: YS
authors.lastname: Gwak
authors.forename: Hee Kee
authors.initials: HK
authors.lastname: Kim
authors.forename: Hee Young
authors.initials: HY
authors.lastname: Kim
authors.forename: Joong Woo
authors.initials: JW
authors.lastname: Leem
mesh_terms: D000818:Animals; D004558:Electric Stimulation; D005073:Evoked Potentials, Somatosensory; D006614:Hindlimb / Q000502:physiology; D008297:Male; D009474:Neurons / Q000502:physiology*; D010146:Pain / Q000503:physiopathology; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D020651:Ventral Thalamic Nuclei / Q000502:physiology*