期刊
JOURNAL OF NEUROSCIENCE
卷 28, 期 46, 页码 11959-11969出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3296-08.2008
关键词
thalamus; excitability; denervation; deafferentation; spinothalamic; calcium channels
资金
- University of Maryland, Baltimore
- National Institute of Neurological Disorders and Stroke [R21 NS055896]
- Integrative Neuroscience Postdoctoral Training [P32 NS07375]
Central pain syndrome (CPS) is defined as pain associated with a lesion of the CNS and is a common consequence of spinal cord injuries. We generated a rodent model of CPS by making unilateral electrolytic or demyelinating lesions centered on the spinothalamic tract in rats. Thermal hyperalgesia and mechanical allodynia occurred in both hind paws and forepaws by 7 d postlesion and were maintained >31 d. Field potentials in the ventral posterior lateral nucleus (VPL) in thalamic brain slices from lesioned animals displayed an increased probability of burst responses. Ethosuximide, a T-type calcium channel blocker, eliminated busting in lesioned thalamic slices and attenuated lesion-induced hyperalgesia and allodynia. We conclude that CPS in this model results from an increase in the excitability of thalamic nuclei that have lost normal ascending inputs as the result of a spinal cord injury and suggest that ethosuximide will relieve human CPS by restoring normal thalamic excitability.
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