The Journal of Neuroscience, November 12, 2008, 28(46):11959-11969; doi:10.1523/JNEUROSCI.3296-08.2008
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Neurobiology of Disease
Maladaptive Homeostatic Plasticity in a Rodent Model of Central Pain Syndrome: Thalamic Hyperexcitability after Spinothalamic Tract Lesions
Gexin Wang1,2 and
Scott M. Thompson1
1Department of Physiology and 2Center for Integrative Neuroscience Training Program, University of Maryland School of Medicine, Baltimore, Maryland 21201
Correspondence should be addressed to Gexin Wang at the above address. Email: gwang003{at}umaryland.edu
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.
Key words: thalamus; excitability; denervation; deafferentation; spinothalamic; calcium channels
Received July 15, 2008;
revised Aug. 25, 2008;
accepted Sept. 23, 2008.
Correspondence should be addressed to Gexin Wang at the above address. Email: gwang003{at}umaryland.edu
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