A quantitative study of neuropeptide immunoreactive cell bodies of primary afferent sensory neurons following rat sciatic nerve peripheral axotomy
Following peripheral axotomy, fluoride resistant acid phosphatase (FRAP) and most neuropeptides are depleted in the central terminals of axotomised nerves and reduced in their corresponding cell bodies (DRG) but vasoactive intestinal polypeptide (VIP) increases. The increase in VIP probably results...
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Veröffentlicht in: | Regulatory peptides 1991-07, Vol.35 (1), p.59-72 |
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Sprache: | eng |
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Zusammenfassung: | Following peripheral axotomy, fluoride resistant acid phosphatase (FRAP) and most neuropeptides are depleted in the central terminals of axotomised nerves and reduced in their corresponding cell bodies (DRG) but vasoactive intestinal polypeptide (VIP) increases. The increase in VIP probably results from a change in gene expression in other ganglion cells which do not normally express VIP. A quantitative study was performed to investigate the proportion of DRG cells immunoreactive for different peptides at increasing times after sciatic nerve section. Retrograde fluorescent neuronal labelling of sciatic nerve cell bodies by injection of fast blue into the proximal stump was combined with unlabelled antibody immunohistochemistry for CGRP and VIP. The proportion of cells immunoreactive for these peptides was quantified between two and fourteen days post-axotomy.
The number of VIP immunoreactive profiles increased significantly in the first 4 days post-axotomy, followed by a slight decrease before rising again. In contrast, the number of and CGRP-immunoreactive cell profiles declined to zero by 14 days post-axotomy. 4 days post-axotomy 50% of VIP positive cells were also immunoreactive for CGRP. There was neither colocalisation between VIP and FRAP nor between CGRP and FRAP.
It is concluded that many peptidergic DRG cell bodies switch their expression of peptide to VIP after injury, whereas non-peptide-containing subpopulations do not. |
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ISSN: | 0167-0115 1873-1686 |
DOI: | 10.1016/0167-0115(91)90254-E |