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Conference Paper: Antisense oligodeoxynucleotide (ODN) against neuronal NOS down-regulated the de novo expression of NOS and decreased the survival of adult spinal motoneurons following root avulsion

TitleAntisense oligodeoxynucleotide (ODN) against neuronal NOS down-regulated the de novo expression of NOS and decreased the survival of adult spinal motoneurons following root avulsion
Authors
KeywordsRoot avulsion
Motoneurons
Nitric oxide synthase
Antisense
Issue Date2003
PublisherSociety for Neuroscience.
Citation
The 33rd Annual Meeting of the Society for Neuroscience (Neuroscience 2003), New Orleans, LA., 8-12 November 2003. How to Cite?
AbstractWe have previously shown that nNOS is de novo expressed in adult spinal motoneurons after root avulsion. Two hypotheses have been proposed to interpret such expression. One is that injury-induced nNOS is neurotoxic and directly responsible for the death of injured neurons. Alternative hypothesis is that induction of nNOS represents an attempt of injured motoneurons to resist an unknown substance that causes the death of motoneurons. In the present study antisense ODN against nNOS was applied in root avulsion model and its effect on nNOS expression and motoneuron survival were observed. Two weeks after C7 root avulsion in adult rats, antisense nNOS ODN was applied intrathecally (4 nmol/each time, repeat in every 3 days). Randomized ODNs set was used as sham control. The nNOS immunocytochemistry, NADPH-d histochemistry and neutral red counter stain were used to assess the effect of treatments. Our result showed that treatments with randomized ODNs set did not alter the expression of nNOS or the survival rate of motoneurons as compared with the control (avulsion only). In contrast, treatment with antisense nNOS ODN significantly down-regulated the expression of nNOS and the number of nNOS positive motoneurons significantly decreased as compared with the control (19.22% vs 55.92% by 3 weeks and 11.48% vs 32.27% by 4 weeks post-injury respectively). At the same time, the treatment significantly reduced the number of survival motoneurons as compared with the control (57.45% vs 76.78% by 3 weeks and 35.44% vs 61.59% by 4 weeks post-injury respectively). Results of the present study support the hypothesis that injury-induced nNOS in injured spinal motoneurons plays a beneficial role on the survival of spinal motoneurons. Supported by The Hong Kong Research Grants Council
DescriptionPresentation no. 602.1
Persistent Identifierhttp://hdl.handle.net/10722/95105

 

DC FieldValueLanguage
dc.contributor.authorZhou, Len_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-25T15:51:48Z-
dc.date.available2010-09-25T15:51:48Z-
dc.date.issued2003en_HK
dc.identifier.citationThe 33rd Annual Meeting of the Society for Neuroscience (Neuroscience 2003), New Orleans, LA., 8-12 November 2003.en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95105-
dc.descriptionPresentation no. 602.1-
dc.description.abstractWe have previously shown that nNOS is de novo expressed in adult spinal motoneurons after root avulsion. Two hypotheses have been proposed to interpret such expression. One is that injury-induced nNOS is neurotoxic and directly responsible for the death of injured neurons. Alternative hypothesis is that induction of nNOS represents an attempt of injured motoneurons to resist an unknown substance that causes the death of motoneurons. In the present study antisense ODN against nNOS was applied in root avulsion model and its effect on nNOS expression and motoneuron survival were observed. Two weeks after C7 root avulsion in adult rats, antisense nNOS ODN was applied intrathecally (4 nmol/each time, repeat in every 3 days). Randomized ODNs set was used as sham control. The nNOS immunocytochemistry, NADPH-d histochemistry and neutral red counter stain were used to assess the effect of treatments. Our result showed that treatments with randomized ODNs set did not alter the expression of nNOS or the survival rate of motoneurons as compared with the control (avulsion only). In contrast, treatment with antisense nNOS ODN significantly down-regulated the expression of nNOS and the number of nNOS positive motoneurons significantly decreased as compared with the control (19.22% vs 55.92% by 3 weeks and 11.48% vs 32.27% by 4 weeks post-injury respectively). At the same time, the treatment significantly reduced the number of survival motoneurons as compared with the control (57.45% vs 76.78% by 3 weeks and 35.44% vs 61.59% by 4 weeks post-injury respectively). Results of the present study support the hypothesis that injury-induced nNOS in injured spinal motoneurons plays a beneficial role on the survival of spinal motoneurons. Supported by The Hong Kong Research Grants Council-
dc.languageengen_HK
dc.publisherSociety for Neuroscience.-
dc.relation.ispartofNeuroscience 2003en_HK
dc.subjectRoot avulsion-
dc.subjectMotoneurons-
dc.subjectNitric oxide synthase-
dc.subjectAntisense-
dc.titleAntisense oligodeoxynucleotide (ODN) against neuronal NOS down-regulated the de novo expression of NOS and decreased the survival of adult spinal motoneurons following root avulsionen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailZhou, L: zlhua62@yahoo.com.cnen_HK
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.identifier.hkuros95296en_HK

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