HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 99/6/3151    most recent 01031.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Jagodic, M. M. Articles by Todorovic, S. M. PubMed PubMed Citation Articles by Jagodic, M. M. Articles by Todorovic, S. M.

REPORT

Upregulation of the T-Type Calcium Current in Small Rat Sensory Neurons After Chronic Constrictive Injury of the Sciatic Nerve

Departments of ¹Anesthesiology, ²Neuroscience and ³Neuroscience Graduate Program, University of Virginia Health System, Charlottesville, Virginia; and ⁴Department of Anesthesiology and Pain Medicine, InJe University, Sanggyepaik Hospital, Seoul, South Korea

Submitted 17 September 2007; accepted in final form 16 April 2008

Recent data indicate that peripheral T-type Ca²⁺ channels are instrumental in supporting acute pain transmission. However, the function of these channels in chronic pain processing is less clear. To address this issue, we studied the expression of T-type Ca²⁺ currents in small nociceptive dorsal root ganglion (DRG) cells from L_4-5 spinal ganglia of adult rats with neuropathic pain due to chronic constrictive injury (CCI) of the sciatic nerve. In control rats, whole cell recordings revealed that T-type currents, measured in 10 mM Ba²⁺ as a charge carrier, were present in moderate density (20 ± 2 pA/pF). In rats with CCI, T-type current density (30 ± 3 pA/pF) was significantly increased, but voltage- and time-dependent activation and inactivation kinetics were not significantly different from those in controls. CCI-induced neuropathy did not significantly change the pharmacological sensitivity of T-type current in these cells to nickel. Collectively, our results indicate that CCI-induced neuropathy significantly increases T-type current expression in small DRG neurons. Our finding that T-type currents are upregulated in a CCI model of peripheral neuropathy and earlier pharmacological and molecular studies suggest that T-type channels may be potentially useful therapeutic targets for the treatment of neuropathic pain associated with partial mechanical injury to the sciatic nerve.