Testosterone effects on ribosomal RNA levels in injured peripheral motor neurons

A preliminary report

Nancy B. Kinderman, Kathryn Jones

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

We have previously demonstrated that administration of testosterone to hamsters during the eary phases of axonal regeneration following facial nerve injury accelerates both the rate of regeneration of the fastest growing population of axons and the return of functional movement. We hypothesized from those studies that testosterone primes the neuronal cell body in such a way as to accelerate the "switch" from a normal to a reparative state. That hypothesis was tested in this study using ribosomal DNA (rDNA) probes in conjunction with in situ hybridization to map the molecular response of the polymerase I system to axotomy, with and without hormone exposure. Adult male hamsters were subjected to right facial nerve severance, with the left side serving as an internal control. Half the animals were administered testosterone propionate via subcutaneous implants. In situ hybridization using a genomic rDNA probe complementary to the 28S rRNA species was accomplished, and levels of rRNA in injured facial neurons assessed both qualitatively and quantitatively. Our initial findings indicate that testosterone markedly upregulates rRNA levels after injury, and support the hypothesis of an acceleration in the metabolic switch to a reparative state. This leads us, in turn, to suggest that this effect of testosterone on the ribosomal system is causally related to the increase in axonal regeneration rate andreturn of functional movement previously documented in this system.

Original languageEnglish (US)
Pages (from-to)157-164
Number of pages8
JournalMetabolic Brain Disease
Volume6
Issue number3
DOIs
StatePublished - Sep 1991
Externally publishedYes

Fingerprint

Ribosomal RNA
Motor Neurons
Neurons
Testosterone
Regeneration
DNA Probes
Ribosomal DNA
Cricetinae
In Situ Hybridization
Facial Nerve Injuries
Switches
Testosterone Propionate
Axotomy
Facial Nerve
Axons
Animals
Up-Regulation
Cells
Hormones
Wounds and Injuries

Keywords

  • axotomy
  • facial motoneuron
  • neurotrophic factor
  • peripheral neuron
  • polymerase I
  • Testosterone propionate

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Biochemistry

Cite this

Testosterone effects on ribosomal RNA levels in injured peripheral motor neurons : A preliminary report. / Kinderman, Nancy B.; Jones, Kathryn.

In: Metabolic Brain Disease, Vol. 6, No. 3, 09.1991, p. 157-164.

Research output: Contribution to journalArticle

@article{eb560d939fda4bd1ab9e56c1d3f5718c,
title = "Testosterone effects on ribosomal RNA levels in injured peripheral motor neurons: A preliminary report",
abstract = "We have previously demonstrated that administration of testosterone to hamsters during the eary phases of axonal regeneration following facial nerve injury accelerates both the rate of regeneration of the fastest growing population of axons and the return of functional movement. We hypothesized from those studies that testosterone primes the neuronal cell body in such a way as to accelerate the {"}switch{"} from a normal to a reparative state. That hypothesis was tested in this study using ribosomal DNA (rDNA) probes in conjunction with in situ hybridization to map the molecular response of the polymerase I system to axotomy, with and without hormone exposure. Adult male hamsters were subjected to right facial nerve severance, with the left side serving as an internal control. Half the animals were administered testosterone propionate via subcutaneous implants. In situ hybridization using a genomic rDNA probe complementary to the 28S rRNA species was accomplished, and levels of rRNA in injured facial neurons assessed both qualitatively and quantitatively. Our initial findings indicate that testosterone markedly upregulates rRNA levels after injury, and support the hypothesis of an acceleration in the metabolic switch to a reparative state. This leads us, in turn, to suggest that this effect of testosterone on the ribosomal system is causally related to the increase in axonal regeneration rate andreturn of functional movement previously documented in this system.",
keywords = "axotomy, facial motoneuron, neurotrophic factor, peripheral neuron, polymerase I, Testosterone propionate",
author = "Kinderman, {Nancy B.} and Kathryn Jones",
year = "1991",
month = "9",
doi = "10.1007/BF00996907",
language = "English (US)",
volume = "6",
pages = "157--164",
journal = "Metabolic Brain Disease",
issn = "0885-7490",
publisher = "Springer New York",
number = "3",

}

TY - JOUR

T1 - Testosterone effects on ribosomal RNA levels in injured peripheral motor neurons

T2 - A preliminary report

AU - Kinderman, Nancy B.

AU - Jones, Kathryn

PY - 1991/9

Y1 - 1991/9

N2 - We have previously demonstrated that administration of testosterone to hamsters during the eary phases of axonal regeneration following facial nerve injury accelerates both the rate of regeneration of the fastest growing population of axons and the return of functional movement. We hypothesized from those studies that testosterone primes the neuronal cell body in such a way as to accelerate the "switch" from a normal to a reparative state. That hypothesis was tested in this study using ribosomal DNA (rDNA) probes in conjunction with in situ hybridization to map the molecular response of the polymerase I system to axotomy, with and without hormone exposure. Adult male hamsters were subjected to right facial nerve severance, with the left side serving as an internal control. Half the animals were administered testosterone propionate via subcutaneous implants. In situ hybridization using a genomic rDNA probe complementary to the 28S rRNA species was accomplished, and levels of rRNA in injured facial neurons assessed both qualitatively and quantitatively. Our initial findings indicate that testosterone markedly upregulates rRNA levels after injury, and support the hypothesis of an acceleration in the metabolic switch to a reparative state. This leads us, in turn, to suggest that this effect of testosterone on the ribosomal system is causally related to the increase in axonal regeneration rate andreturn of functional movement previously documented in this system.

AB - We have previously demonstrated that administration of testosterone to hamsters during the eary phases of axonal regeneration following facial nerve injury accelerates both the rate of regeneration of the fastest growing population of axons and the return of functional movement. We hypothesized from those studies that testosterone primes the neuronal cell body in such a way as to accelerate the "switch" from a normal to a reparative state. That hypothesis was tested in this study using ribosomal DNA (rDNA) probes in conjunction with in situ hybridization to map the molecular response of the polymerase I system to axotomy, with and without hormone exposure. Adult male hamsters were subjected to right facial nerve severance, with the left side serving as an internal control. Half the animals were administered testosterone propionate via subcutaneous implants. In situ hybridization using a genomic rDNA probe complementary to the 28S rRNA species was accomplished, and levels of rRNA in injured facial neurons assessed both qualitatively and quantitatively. Our initial findings indicate that testosterone markedly upregulates rRNA levels after injury, and support the hypothesis of an acceleration in the metabolic switch to a reparative state. This leads us, in turn, to suggest that this effect of testosterone on the ribosomal system is causally related to the increase in axonal regeneration rate andreturn of functional movement previously documented in this system.

KW - axotomy

KW - facial motoneuron

KW - neurotrophic factor

KW - peripheral neuron

KW - polymerase I

KW - Testosterone propionate

UR - http://www.scopus.com/inward/record.url?scp=0026348821&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026348821&partnerID=8YFLogxK

U2 - 10.1007/BF00996907

DO - 10.1007/BF00996907

M3 - Article

VL - 6

SP - 157

EP - 164

JO - Metabolic Brain Disease

JF - Metabolic Brain Disease

SN - 0885-7490

IS - 3

ER -