TGF-beta 2 attenuates the injury-induced death of mature motoneurons

J Neurosci Res. 2000 Dec 15;62(6):809-13. doi: 10.1002/1097-4547(20001215)62:6<809::AID-JNR7>3.0.CO;2-4.

Abstract

The distributions of transforming growth factor-betas (TGF-betas) and their receptors suggest that the TGF-betas regulate motoneuron survival. This hypothesis was tested by avulsing the hypoglossal nerve of adult rats and perfusing either TGF-beta 2 or vehicle adjacent to the hypoglossal nucleus. By 4 weeks, half of the avulsed motoneurons had died. Infusion of 6 ng of TGF-beta 2 adjacent to the avulsed motor nucleus caused a significant attenuation of this death. This dose of TGF-beta 2 is low compared to that used with GDNF or BDNF in previous studies of avulsed motoneurons, indicating that TGF-beta 2 may be one of the more potent survival factors for adult motoneurons. TGF-beta 2 was, however, unable to prevent or reduce the axotomy-induced down regulation of choline acetyltransferase. Other motoneuron survival factors also have a narrow-spectrum of actions, suggesting that the homeostasis of motoneurons is regulated by a cocktail of growth factors with distinct but partially overlapping actions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axotomy
  • Cell Death / drug effects*
  • Cell Death / physiology
  • Choline O-Acetyltransferase / drug effects*
  • Choline O-Acetyltransferase / metabolism
  • Female
  • Hypoglossal Nerve / drug effects*
  • Hypoglossal Nerve / physiology
  • Hypoglossal Nerve Injuries
  • Male
  • Motor Neurons / drug effects*
  • Motor Neurons / physiology
  • Rats
  • Transforming Growth Factor beta / pharmacology*
  • Transforming Growth Factor beta2

Substances

  • Transforming Growth Factor beta
  • Transforming Growth Factor beta2
  • Choline O-Acetyltransferase