NDLI: Fifth lumbar spinal nerve injury causes neurochemical changes in corresponding as well as adjacent spinal segments: a possible mechanism underlying neuropathic pain.

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Fifth lumbar spinal nerve injury causes neurochemical changes in corresponding as well as adjacent spinal segments: a possible mechanism underlying neuropathic pain.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Shehab, Safa Al-Deen Saudi
Description	Author Affiliation: Shehab SA ( Department of Anatomy, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain, PO BOX 16777, United Arab Emirates. Electronic address: s.shehab@uaeu.ac.ae.)
Abstract	Previous investigations of the anatomical basis of the neuropathic-like manifestations in the spinal nerve ligation animal model have shown that the central terminations of the unmyelinated primary afferents of L5 spinal nerve are not restricted to the corresponding L5 spinal segment, and rather extend to two spinal segments rostrally and one segment caudally where they intermingle with primary afferents of the adjacent L4 spinal nerve. The aim of the present study was to investigate the neurochemical changes in the dorsal horn of the spinal cord and DRGs after L5 nerve injury in rats. In the first experiment, the right L5 nerve was ligated and sectioned for 14 days, and isolectin B4 (IB4, a tracer for unmyelinated primary afferents) was injected into the left L5 nerve. The results showed that the vasoactive intestinal peptide (VIP) was up-regulated in laminae I-II of L3-L6 spinal segments on the right side in exactly the same areas where IB4 labelled terminals were revealed on the left side. In the second experiment, L5 was ligated and sectioned and the spinal cord and DRGs were stained immunocytochemically with antibodies raised against various peptides known to be involved in pain transmission and hyperalgesia. The results showed that L5 nerve lesion caused down-regulation of substance P, calcitonin-gene related peptide and IB4 binding and up-regulation of neuropeptide Y and neurokinin-1 receptor in the dorsal horn of L4 and L5 spinal segments. Similar neurochemical changes were observed only in the corresponding L5 DRG with minimal effects observed in L3, L4 and L6 DRGs. Although, L5 nerve injury caused an up-regulation in NPY, no change in SP and CGRP immunoreactivity was observed in ipsilateral garcile nucleus. These neuroplastic changes in the dorsal horn of the spinal cord, in the adjacent uninjured territories of the central terminations of the adjacent uninjured nerves, might explain the mechanism of hyperalgesia after peripheral nerve injury.
File Format	HTM / HTML
ISSN	08910618
Volume Number	55
e-ISSN	18736300
Journal	Journal of Chemical Neuroanatomy
Language	English
Publisher	Elsevier
Publisher Date	2014-01-01
Publisher Place	Netherlands
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Neurology Discipline Chemistry Discipline Anatomy Neuralgia Metabolism Peripheral Nerve Injuries Spinal Cord Spinal Nerves Injuries Animals Lumbar Vertebrae Etiology Neuropeptide Y Complications Rats Rats, Wistar Receptors, Neurokinin-1 Substance P Up-regulation Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cellular and Molecular Neuroscience

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