Differential expression of mRNAs for neurotrophins and their receptors after axotomy of the sciatic nerve.

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  • Additional Information
    • Source:
      Publisher: Rockefeller University Press Country of Publication: United States NLM ID: 0375356 Publication Model: Print Cited Medium: Print ISSN: 0021-9525 (Print) Linking ISSN: 00219525 NLM ISO Abbreviation: J Cell Biol Subsets: MEDLINE
    • Publication Information:
      Original Publication: New York : Rockefeller University Press
    • Subject Terms:
      Nerve Growth Factors/*genetics ; RNA, Messenger/*analysis ; Receptors, Nerve Growth Factor/*genetics ; Sciatic Nerve/*chemistry; Animals ; Axons/chemistry ; Axons/ultrastructure ; Brain Chemistry ; Brain-Derived Neurotrophic Factor ; In Situ Hybridization ; Male ; Membrane Proteins/analysis ; Membrane Proteins/genetics ; Models, Biological ; Muscles/chemistry ; Muscles/ultrastructure ; Nerve Growth Factors/analysis ; Nerve Tissue Proteins/analysis ; Nerve Tissue Proteins/genetics ; Neurons/chemistry ; Neurons/ultrastructure ; Neurotrophin 3 ; RNA, Messenger/genetics ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/analysis ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor, Ciliary Neurotrophic Factor ; Receptor, trkC ; Receptors, Growth Factor/analysis ; Receptors, Growth Factor/genetics ; Receptors, Nerve Growth Factor/analysis ; Sciatic Nerve/surgery ; Sciatic Nerve/ultrastructure ; Spinal Cord/chemistry ; Spinal Cord/ultrastructure ; Time Factors
    • Abstract:
      The neurotrophin family includes NGF, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). Previous studies have demonstrated that expression of NGF and its low-affinity receptor is induced in nonneuronal cells of the distal segment of the transected sciatic nerve suggesting a role for NGF during axonal regeneration (Johnson, E. M., M. Taniuchi, and P. S. DeStefano. 1988. Trends Neurosci. 11:299-304). To assess the role of the other neurotrophins and the members of the family of Trk signaling neurotrophin receptors, we have here quantified the levels of mRNAs for BDNF, NT-3, and NT-4 as well as mRNAs for trkA, trkB, and trkC at different times after transection of the sciatic nerve in adult rats. A marked increase of BDNF and NT-4 mRNAs in the distal segment of the sciatic nerve was seen 2 wk after the lesion. The increase in BDNF mRNA was mediated by a selective activation of the BDNF exon IV promoter and adrenalectomy attenuated this increase by 50%. NT-3 mRNA, on the other hand, decreased shortly after the transection but returned to control levels 2 wk later. In Schwann cells ensheathing the sciatic nerve, only trkB mRNA encoding truncated TrkB receptors was detected with reduced levels in the distal part of the lesioned nerve. Similar results were seen using a probe that detects all forms of trkC mRNA. In the denervated gastrocnemius muscle, the level of BDNF mRNA increased, NT-3 mRNA did not change, while NT-4 mRNA decreased. In the spinal cord, only small changes were seen in the levels of neutrophin and trk mRNAs. These results show that expression of mRNAs for neurotrophins and their Trk receptors is differentially regulated after a peripheral nerve injury. Based on these results a model is presented for how the different neurotrophins could cooperate to promote regeneration of injured peripheral nerves.
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    • Grant Information:
      AG04418 United States AG NIA NIH HHS; NS09199 United States NS NINDS NIH HHS
    • Accession Number:
      0 (Brain-Derived Neurotrophic Factor)
      0 (Membrane Proteins)
      0 (Nerve Growth Factors)
      0 (Nerve Tissue Proteins)
      0 (Neurotrophin 3)
      0 (RNA, Messenger)
      0 (Receptor, Ciliary Neurotrophic Factor)
      0 (Receptors, Growth Factor)
      0 (Receptors, Nerve Growth Factor)
      EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
      EC 2.7.10.1 (Receptor, trkC)
      P658DCA9XD (neurotrophin 4)
    • Publication Date:
      Date Created: 19931001 Date Completed: 19931119 Latest Revision: 20220330
    • Publication Date:
      20231215
    • Accession Number:
      PMC2119843
    • Accession Number:
      10.1083/jcb.123.2.455
    • Accession Number:
      8408225