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|Title:||The role of nitric oxide in facial motoneuronal death|
|Authors:||Ruan, R.-S. |
|Keywords:||Facial motor neuron|
Facial nerve avulsion
|Source:||Ruan, R.-S.,Leong, S.-K.,Yeoh, K.-H. (1995). The role of nitric oxide in facial motoneuronal death. Brain Research 698 (1-2) : 163-168. ScholarBank@NUS Repository. https://doi.org/10.1016/0006-8993(95)00887-V|
|Abstract:||The present study aimed to determine whether nitric oxide synthase (NOS)/nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) activity would be induced in facial motoneurons after facial nerve avulsion and if so, whether such activity was related to neuronal death commonly observed after such injury. The left facial nerve in each of 28 Wistar albino rats was avulsed from the facial canal. Ten of them received either daily injections of N(ω)-nitro-L-arginine methyl ether (L-NAME) or the vehicle. After survival time ranging from 2-50 days, serial brainstem sections were processed for NOS immunocytochemistry and NADPH-d histochemistry respectively. The number of surviving, NOS and NADPH-d positive and NOS negative neurons were compared statistically. Two days after facial nerve avulsion, increased NADPH-d activity was noticed in the facial motoneurons and in the endothelial lining of man dilated blood vessels in the facial motor nucleus (FMN). NOS-positive neurons were not detectable until five days after operation. Both the number and staining intensity of NADPH-d and NOS-positive neurons increased steadily with increasing survival time while the number of surviving neurons decreased after nerve avulsion. Daily administration of L-NAME protected 17% the neurons from death in the affected FMN when examined at 30 days after nerve avulsion, suggesting a neurodestructive property of NO. It was also noticed that some of the surviving neurons were first NOS positive but became NOS negative later.|
|Source Title:||Brain Research|
|Appears in Collections:||Staff Publications|
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