IMPORTANCE OF TARGET INNERVATION IN RECOVERY FROM AXOTOMY-INDUCED LOSS OF ANDROGEN RECEPTOR IN RAT PERINEAL MOTONEURONS

Citation
Ha. Alshamma et Ap. Arnold, IMPORTANCE OF TARGET INNERVATION IN RECOVERY FROM AXOTOMY-INDUCED LOSS OF ANDROGEN RECEPTOR IN RAT PERINEAL MOTONEURONS, Journal of neurobiology, 28(3), 1995, pp. 341-353
Citations number
42
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00223034
Volume
28
Issue
3
Year of publication
1995
Pages
341 - 353
Database
ISI
SICI code
0022-3034(1995)28:3<341:IOTIIR>2.0.ZU;2-B
Abstract
In adult male rats, axotomy of the spinal nucleus of the bulbocavernos us (SNB) motoneurons transiently downregulates androgen receptor (AR) immunoreactivity. The present study investigates the importance of tar get reinnervation in the recovery of AR expression in axotomized SNB m otoneurons after short(up to 5 days) and long (1 to 6 weeks) periods o f recovery. In the long-term recovery experiment, animals were divided into two groups, In one, the two stumps of the cut pudendal nerve, wh ich carries the axons of the SNB motoneurons, were sutured together im mediately after axotomy. In the second group, the proximal stump was l igated immediately after axotomy to prevent target reinnervation, Axot omy of the SNB motoneurons caused a significant down-regulation in AR immunoreactivity within 3 days, At 6 weeks, AR immunoreactivity was st ill depressed in ligated animals but had recovered to control levels i n resutured animals, The recovery in the resutured group was coinciden t with the first signs of reinnervation of the target perineal muscles , although reinnervation seemed to lag behind AR immunoreactivity. SNB soma size was significantly reduced 2 weeks after axotomy and returne d to control levels after 6 weeks of recovery only in the resutured an imals, These findings suggest that the target perineal muscles play a role in the regulation of AR expression and androgen sensitivity in th e SNB motoneurons, perhaps mediated by muscle-derived trophic factors. (C) 1995 John Wiley & Sons, Inc.