4.5 Article

Effects of spinal nerve ligation on immunohistochemically identified neurons in the L4 and L5 dorsal root ganglia of the rat

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JOURNAL OF COMPARATIVE NEUROLOGY
卷 475, 期 4, 页码 575-589

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WILEY
DOI: 10.1002/cne.20209

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nerve injury; calcitonin gene-related peptide; N52; isolectin B4; neuropathic pain; allodynia

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This study examined the effect of spinal nerve ligation on different populations of immunohistochemically identified neurons in the dorsal root ganglia (DRG) of the rat. The optical fractionator method was used to count neurons in the ipsilateral L4 and L5 DRG 1-20 weeks after ligation of the L5 and L6 spinal nerves, sham surgery, or no surgery. One week after ligation, neurons in the L5 DRG that were labeled by 1134, a marker of unmyelinated primary afferent neurons, were largely absent. The numbers of IB4-labeled neurons then progressively increased to reach control values by 20 weeks. A smaller, sustained decrease occurred in the number of small-, medium- and large-sized neurons immunoreactive for calcitonin gene-related peptide (CGRP), a marker for peptidergic primary afferents, in the L5 DRG. There was a proportionately greater decrease in the numbers of medium- to large-sized CGRP-like immunoreactive neurons. The number of myelinated afferents in the L5 DRG, identified by their staining for neurofilament protein (N52), did not change after ligation. However, closer examination revealed a significant decrease in the numbers of large-sized neurons, coupled with an increase in the numbers of small- to medium-sized neurons, and the appearance of a novel population of very small-sized neurons labeled by N52. The numbers and cell size distributions of IB4-labeled, CGRP-like immunoreactive, and N52-labeled neurons were unchanged in the adjacent L4 DRG. Unlike the L5 DRG, injury-induced changes in the expression of various receptors, neurotransmitters and neurotrophic factors in the L4 DRG are not confounded by a change in the immunohistochemical phenotype of primary afferent neurons. (C) 2004 Wiley-Liss, Inc.

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