The role of capsacin injury on nerve morphology & pain
Project Number1F32NS047002-01
Contact PI/Project LeaderSCHWARZ, JACOB P
Awardee OrganizationJOHNS HOPKINS UNIVERSITY
Description
Abstract Text
DESCRIPTION (provided by applicant):
The mechanisms underlying neuropathic pain remain incompletely understood. Using a modification of the spinal nerve ligation model of Chung, have observed: 1) hyperalgesia is not reversed by dorsal rhizotomy, 2) spontaneous activity develops among C fibers of adjacent, uninjured roots, 3) prominent remodeling of Remak bundles containing surviving C fibers in distal branches. We hypothesize that selective lesion of L5 nerve leads to Wallerian degeneration distally and partial Remak bundle denervation. Remak, bundles react as if completely denervated and release excessive growth factors and cytokines. Intact L4 fibers transport these agents to nerve cell bodies they induce changes in excitability and hyperalgesia. In the proposed study, capsacin will be applied to the L5 mixed spinal root. This technique will provide a selective lesion of nociceptive afferents and elaborate the role of this lesion in hyperalgesia, Remak bundle remodeling, and spontaneous activity in the uninjured fibers. This will clarify neuropathic pain phenomena.
National Institute of Neurological Disorders and Stroke
CFDA Code
853
DUNS Number
001910777
UEI
FTMTDMBR29C7
Project Start Date
01-July-2003
Project End Date
30-June-2005
Budget Start Date
01-July-2003
Budget End Date
30-June-2004
Project Funding Information for 2003
Total Funding
$49,864
Direct Costs
$49,864
Indirect Costs
Year
Funding IC
FY Total Cost by IC
2003
National Institute of Neurological Disorders and Stroke
$49,864
Year
Funding IC
FY Total Cost by IC
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