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Restoration of substance P and calcitonin gene-related peptide in dorsal root ganglia and dorsal horn after neonatal sciatic nerve lesion.
J Comp Neurol. 1993 Aug 15; 334(3):370-84.JC

Abstract

Dorsal root ganglion (DRG) neurons decrease their substance P (SP) synthesis after peripheral nerve lesions. Levels in the dorsal horn also decline but return to normal if regeneration is successful. In adults, when regeneration is prevented, recovery of SP in the dorsal horn is slow and incomplete, whereas in newborns, recovery is rapid and complete even though retrograde cell death of DRG neurons is greater than in adults. We have examined the mechanisms that might account for the rapid and complete recovery of SP and calcitonin-gene related peptide (CGRP) in the dorsal horn after peripheral nerve injury in newborns. Peptides were compared in the L4 and L5 DRG and spinal cord segments of normal rats and in rats surviving 6 days to 4 months after sciatic nerve section/ligation within 24 hours of birth. Sciatic nerve section/ligation produced 50% neuron death in L4 and L5 DRGs, but immunocytochemical methods showed that both SP-immunoreactivity (-IR) and CGRP-IR recovered completely in dorsal horn. Radioimmunoassay confirmed that recovery of SP was not an artefact due to shrinkage. beta-Preprotachykinin (PPT)-mRNA hybridization and SP-IR were observed mostly in small neurons; alpha-CGRP-mRNA-hybridized and CGRP-IR neurons were more heterogeneous. The percentage of DRG neurons that contained SP (approximately 25%) or CGRP (approximately 50%) was the same in normal newborn and adult rats. Neither selective cell survival nor change in neuron phenotype was likely to contribute to the recovery seen in the dorsal horn, and DRG neurons ipsilateral to the lesion exhibited the same level of hybridized beta-PPT-mRNA and alpha-CGRP-mRNA as intact DRG neurons. Because neither the constitutive level of expression of the genes nor peptide levels increased above those observed in intact DRG neurons, these mechanisms were also not responsible. Axotomized DRG neurons, however, contributed to recovery. Recovery was also due to sprouting by neurons in intact DRGs rostral and caudal to L4 and L5.

Authors+Show Affiliations

Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

7690784

Citation

Nothias, F, et al. "Restoration of Substance P and Calcitonin Gene-related Peptide in Dorsal Root Ganglia and Dorsal Horn After Neonatal Sciatic Nerve Lesion." The Journal of Comparative Neurology, vol. 334, no. 3, 1993, pp. 370-84.
Nothias F, Tessler A, Murray M. Restoration of substance P and calcitonin gene-related peptide in dorsal root ganglia and dorsal horn after neonatal sciatic nerve lesion. J Comp Neurol. 1993;334(3):370-84.
Nothias, F., Tessler, A., & Murray, M. (1993). Restoration of substance P and calcitonin gene-related peptide in dorsal root ganglia and dorsal horn after neonatal sciatic nerve lesion. The Journal of Comparative Neurology, 334(3), 370-84.
Nothias F, Tessler A, Murray M. Restoration of Substance P and Calcitonin Gene-related Peptide in Dorsal Root Ganglia and Dorsal Horn After Neonatal Sciatic Nerve Lesion. J Comp Neurol. 1993 Aug 15;334(3):370-84. PubMed PMID: 7690784.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Restoration of substance P and calcitonin gene-related peptide in dorsal root ganglia and dorsal horn after neonatal sciatic nerve lesion. AU - Nothias,F, AU - Tessler,A, AU - Murray,M, PY - 1993/8/15/pubmed PY - 1993/8/15/medline PY - 1993/8/15/entrez SP - 370 EP - 84 JF - The Journal of comparative neurology JO - J. Comp. Neurol. VL - 334 IS - 3 N2 - Dorsal root ganglion (DRG) neurons decrease their substance P (SP) synthesis after peripheral nerve lesions. Levels in the dorsal horn also decline but return to normal if regeneration is successful. In adults, when regeneration is prevented, recovery of SP in the dorsal horn is slow and incomplete, whereas in newborns, recovery is rapid and complete even though retrograde cell death of DRG neurons is greater than in adults. We have examined the mechanisms that might account for the rapid and complete recovery of SP and calcitonin-gene related peptide (CGRP) in the dorsal horn after peripheral nerve injury in newborns. Peptides were compared in the L4 and L5 DRG and spinal cord segments of normal rats and in rats surviving 6 days to 4 months after sciatic nerve section/ligation within 24 hours of birth. Sciatic nerve section/ligation produced 50% neuron death in L4 and L5 DRGs, but immunocytochemical methods showed that both SP-immunoreactivity (-IR) and CGRP-IR recovered completely in dorsal horn. Radioimmunoassay confirmed that recovery of SP was not an artefact due to shrinkage. beta-Preprotachykinin (PPT)-mRNA hybridization and SP-IR were observed mostly in small neurons; alpha-CGRP-mRNA-hybridized and CGRP-IR neurons were more heterogeneous. The percentage of DRG neurons that contained SP (approximately 25%) or CGRP (approximately 50%) was the same in normal newborn and adult rats. Neither selective cell survival nor change in neuron phenotype was likely to contribute to the recovery seen in the dorsal horn, and DRG neurons ipsilateral to the lesion exhibited the same level of hybridized beta-PPT-mRNA and alpha-CGRP-mRNA as intact DRG neurons. Because neither the constitutive level of expression of the genes nor peptide levels increased above those observed in intact DRG neurons, these mechanisms were also not responsible. Axotomized DRG neurons, however, contributed to recovery. Recovery was also due to sprouting by neurons in intact DRGs rostral and caudal to L4 and L5. SN - 0021-9967 UR - https://www.unboundmedicine.com/medline/citation/7690784/Restoration_of_substance_P_and_calcitonin_gene_related_peptide_in_dorsal_root_ganglia_and_dorsal_horn_after_neonatal_sciatic_nerve_lesion_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0021-9967&date=1993&volume=334&issue=3&spage=370 DB - PRIME DP - Unbound Medicine ER -