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Cell body response to injury in motoneurons and primary sensory neurons of a mutant mouse, Ola (Wld), in which Wallerian degeneration is delayed.
J Comp Neurol. 1995 Sep 04; 359(4):653-62.JC

Abstract

We examined the response to axon injury in the facial motoneurons and dorsal root ganglion (DRG) neurons of C57BL/Ola (Wld) mice, compared with the responses of C57BL/6J mice. The peripheral nerves of Ola mutants undergo remarkably slowed and muted Wallerian degeneration after injury. The increase in GAP-43 mRNA levels in facial motoneurons and DRG neurons was similar in both strains of mice, as was the initial decrease in medium-weight neurofilament (NFM) mRNA in facial motoneurons, and the increase in JUN immunoreactivity in both types of neurons. However, the subsequent recovery to normal low levels of JUN and GAP-43 mRNA expression and high levels of NFM mRNA was delayed in Ola motoneurons. We ascribe this delay to the slow regeneration and target reinnervation of facial axons in the Ola mice. These results show that absence of rapid Wallerian degeneration does not affect the initial cell body response to axonal injury. They also provide further evidence that restoration of normal levels of expression of GAP-43 and NFM mRNAs is dependent on target reinnervation and/or trophic factors provided by the distal nerve. Impaired regeneration in the Ola mouse does not seem to be a consequence of a defective cell body response to injury, and our results illustrate the general principle that, even if there is a vigorous cell body response to injury, normal axonal regeneration requires the additional provision of a favorable environment for growth.

Authors+Show Affiliations

Department of Physiology, Queen's University, Kingston, Ontario, Canada.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7499554

Citation

Bisby, M A., et al. "Cell Body Response to Injury in Motoneurons and Primary Sensory Neurons of a Mutant Mouse, Ola (Wld), in Which Wallerian Degeneration Is Delayed." The Journal of Comparative Neurology, vol. 359, no. 4, 1995, pp. 653-62.
Bisby MA, Tetzlaff W, Brown MC. Cell body response to injury in motoneurons and primary sensory neurons of a mutant mouse, Ola (Wld), in which Wallerian degeneration is delayed. J Comp Neurol. 1995;359(4):653-62.
Bisby, M. A., Tetzlaff, W., & Brown, M. C. (1995). Cell body response to injury in motoneurons and primary sensory neurons of a mutant mouse, Ola (Wld), in which Wallerian degeneration is delayed. The Journal of Comparative Neurology, 359(4), 653-62.
Bisby MA, Tetzlaff W, Brown MC. Cell Body Response to Injury in Motoneurons and Primary Sensory Neurons of a Mutant Mouse, Ola (Wld), in Which Wallerian Degeneration Is Delayed. J Comp Neurol. 1995 Sep 4;359(4):653-62. PubMed PMID: 7499554.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cell body response to injury in motoneurons and primary sensory neurons of a mutant mouse, Ola (Wld), in which Wallerian degeneration is delayed. AU - Bisby,M A, AU - Tetzlaff,W, AU - Brown,M C, PY - 1995/9/4/pubmed PY - 1995/9/4/medline PY - 1995/9/4/entrez SP - 653 EP - 62 JF - The Journal of comparative neurology JO - J Comp Neurol VL - 359 IS - 4 N2 - We examined the response to axon injury in the facial motoneurons and dorsal root ganglion (DRG) neurons of C57BL/Ola (Wld) mice, compared with the responses of C57BL/6J mice. The peripheral nerves of Ola mutants undergo remarkably slowed and muted Wallerian degeneration after injury. The increase in GAP-43 mRNA levels in facial motoneurons and DRG neurons was similar in both strains of mice, as was the initial decrease in medium-weight neurofilament (NFM) mRNA in facial motoneurons, and the increase in JUN immunoreactivity in both types of neurons. However, the subsequent recovery to normal low levels of JUN and GAP-43 mRNA expression and high levels of NFM mRNA was delayed in Ola motoneurons. We ascribe this delay to the slow regeneration and target reinnervation of facial axons in the Ola mice. These results show that absence of rapid Wallerian degeneration does not affect the initial cell body response to axonal injury. They also provide further evidence that restoration of normal levels of expression of GAP-43 and NFM mRNAs is dependent on target reinnervation and/or trophic factors provided by the distal nerve. Impaired regeneration in the Ola mouse does not seem to be a consequence of a defective cell body response to injury, and our results illustrate the general principle that, even if there is a vigorous cell body response to injury, normal axonal regeneration requires the additional provision of a favorable environment for growth. SN - 0021-9967 UR - https://www.unboundmedicine.com/medline/citation/7499554/Cell_body_response_to_injury_in_motoneurons_and_primary_sensory_neurons_of_a_mutant_mouse_Ola__Wld__in_which_Wallerian_degeneration_is_delayed_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0021-9967&date=1995&volume=359&issue=4&spage=653 DB - PRIME DP - Unbound Medicine ER -