COMPRESSION OF THE FACIAL-NERVE CAUSED INCREASED NITRIC-OXIDE SYNTHASE ACTIVITY IN THE FACIAL MOTOR NUCLEUS

Citation
Pth. Wong et al., COMPRESSION OF THE FACIAL-NERVE CAUSED INCREASED NITRIC-OXIDE SYNTHASE ACTIVITY IN THE FACIAL MOTOR NUCLEUS, Neuroscience, 67(3), 1995, pp. 697-702
Citations number
22
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
67
Issue
3
Year of publication
1995
Pages
697 - 702
Database
ISI
SICI code
0306-4522(1995)67:3<697:COTFCI>2.0.ZU;2-2
Abstract
Nitric oxide synthase activities in the facial motor nucleus were stud ied in rats after unilateral compression of the facial nerve. Using a radiometric assay which measured the total soluble nitric bride syntha se activities in the facial motor nucleus and the surrounding tissues, it was found that nitric oxide synthase activities were markedly incr eased during facial paralysis that resulted from compression of the fa cial nerve. The subsequent decrease in nitric oxide synthase activitie s between postoperative days 20 and 40 coincided with the recovery of facial functions. In contrast, staining with NADPH-diaphorase histoche mistry revealed that the diaphorase activities in the facial motor neu rons were markedly increased between days 20-40 when the total activit ies as measured biochemically were in decline. However, staining of th e vascular endothelium was increased on postoperative day 7 when the t otal activity was high. It is suggested that the increase in total nit ric oxide synthase activities immediately after facial nerve compressi on may be predominantly endothelial. Since the increase in neuronal NA DPH-diaphorase reactivity coincided with the recovery of facial functi ons, increased neuronal nitric oxide synthase may be a contributing fa ctor to the restoration of facial innervation. The results of this stu dy show that biochemical measurements of soluble nitric oxide synthase activities in tissue homogenates and NADPH-diaphorase histochemical s taining in tissue sections may represent two distinct populations of n itric oxide synthase. The former, which may be predominantly endotheli al, increased in the facial motor nucleus immediately after ipsilatera l facial nerve compression during the period of facial paralysis and t hus, may be related to compression-induced neuronal damages. On the ot her hand, the latter, which is neuronal, increased in the facial motor nucleus at a later time period when recovery of facial functions occu rred and thus may be associated with axonal regeneration.