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Abstract

 
Abstract No.:C-D3139
Country:Canada
  
Title:LOSS OF NON-PEPTIDERGIC NOCICEPTIVE FIBERS AND ITS EFFECT ON NK-1 RECEPTOR EXPRESSION BY MORPHOLOGICALLY CHARACTERIZED SPINAL LAMINA I NEURONS
  
Authors/Affiliations:1 Abeer Saeed*; 1 Alfredo Ribeiro-da-Silva;
1 McGill University, Montreal, QC, Canada
  
Content:Objectives: Pain-related information is relayed to the brain by neurokinin-1 receptor (NK-1r)-containing lamina I projection neurons. Previous studies have shown that lamina I projection neurons can be classified into fusiform, pyramidal and multipolar cells. Our laboratory has shown a de novo expression of NK-1r by pyramidal neurons in the CFA-induced arthritis model. Based on this, we deemed it interesting to study whether pyramidal neurons would also express NK-1r in an animal model in which we have previously shown a drastic increase in NK-1r expression but no augmented nociceptive responses.

Materials & Methods: We injected, under anesthesia, the lectin IB4 conjugated to saporin (SAP) into the left sciatic nerve of male Sprague Dawley rats to selectively lesion the non-peptidergic nociceptive C-fibers. Animals were sacrificed from 2 weeks to 2 months post-lesion. Horizontal sections of spinal segments L4 and L5 were cut and processed for IB4 binding and NK-1r immunoreactivity using immunofluorescence.

Results: Examination of IB4-SAP treated rats post-lesion revealed no significant increase in the number of lamina I cells expressing NK-1r of either the fusiform or multipolar types. Moreover, pyramidal cells seldom expressed the NK-1r in both control and lesioned animals. Surprisingly, we also observed a direct innervation of lamina I neurons by IB4-positive, calcitonin gene related peptide (CGRP)-negative neurons in control animals, which did not occur ipsilaterally in lesioned animals.

Conclusions: These observations support the concept that increased activity by the peptidergic nociceptive afferents may be important in the maintenance of nociceptive responses in the absence of non-peptidergic fibers.

Support Contributed By: CIHR grant #79411
  
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