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Alterations in Burst Firing of Thalamic VPL Neurons and Reversal by Na_v1.3 Antisense After Spinal Cord Injury

¹Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven; ²Rehabilitation Research Center, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut; and ³Department of Surgery, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island

Submitted 26 September 2005; accepted in final form 7 February 2006

We recently showed that spinal cord contusion injury (SCI) at the thoracic level induces pain-related behaviors and increased spontaneous discharges, hyperresponsiveness to innocuous and noxious peripheral stimuli, and enlarged receptive fields in neurons in the ventral posterolateral (VPL) nucleus of the thalamus. These changes are linked to the abnormal expression of Na_v1.3, a rapidly repriming voltage-gated sodium channel. In this study, we examined the burst firing properties of VPL neurons after SCI. Adult male Sprague–Dawley rats underwent contusion SCI at the T9 level. Four weeks later, when Na_v1.3 protein was upregulated within VPL neurons, extracellular unit recordings were made from VPL neurons in intact animals, those with SCI, and in SCI animals after receiving lumbar intrathecal injections of Na_v1.3 antisense or mismatch oligodeoxynucleotides for 4 days. After SCI, VPL neurons with identifiable peripheral receptive fields showed rhythmic oscillatory burst firing with changes in discrete burst properties, and alternated among single-spike, burst, silent, and spindle wave firing modes. Na_v1.3 antisense, but not mismatch, partially reversed alterations in burst firing after SCI. These results demonstrate several newly characterized changes in spontaneous burst firing properties of VPL neurons after SCI and suggest that abnormal expression of Na_v1.3 contributes to these phenomena.

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