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Article: Caspase inhibitors promote the survival of avulsed spinal motoneurons in neonatal rats

TitleCaspase inhibitors promote the survival of avulsed spinal motoneurons in neonatal rats
Authors
KeywordsApoptosis
Caspases
Neuronal survival
Spinal motoneurons
Issue Date2001
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.neuroreport.com
Citation
Neuroreport, 2001, v. 12 n. 3, p. 541-545 How to Cite?
AbstractFollowing ventral root avulsion in neonatal animals, the degeneration of spinal motoneurons occurs by an apoptotic-like morphological pathway. In adult animals, however, the mechanism of degeneration of injured motoneurons is still controversial. Because caspases are important mediators of apoptosis, we have investigated the effects of the caspase inhibitors, benzyloxycarbonyl-Asp(OMe)fluoromethylketone (Boc-D-FMK), and N-acetyl-Asp-Glu-Val-Asp aldehyde (Ac-DEVD-CHO) on the survival of neonatal and adult spinal motoneurons after root avulsion of the C7 spinal cord. In the control neonatal animals, virtually all motoneurons had degenerated by 7 days following root avulsion. Treatment with either 0.5 μg Boc-D-FMK or 1 μg Ac-DEVD-CHO enhanced the survival of motoneurons to 80% and 85% for up to 2 weeks post-injury. By 21 days post-injury, 70% of avulsed motoneurons were still present after Boc-D-FMK treatment, whereas all avulsed motoneurons died after treatment with Ac-DEVD-CHO. In adult animals, neither inhibitor was neuroprotective for motoneurons following root avulsion. In summary, the inhibition of caspases effectively rescued avulsed neonatal motoneurons which are died by apoptotic pathway. By contrast, because caspase inhibitors failed to rescue injured motoneurons in adult animals, their death may occur by a non-apoptotic pathway. © 2001 Lippincott Williams & Wilkins.
Persistent Identifierhttp://hdl.handle.net/10722/149604
ISSN
2023 Impact Factor: 1.6
2023 SCImago Journal Rankings: 0.459
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, YMen_US
dc.contributor.authorWu, Wen_US
dc.contributor.authorYip, HKen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorOppenheim, RWen_US
dc.date.accessioned2012-06-26T05:55:49Z-
dc.date.available2012-06-26T05:55:49Z-
dc.date.issued2001en_US
dc.identifier.citationNeuroreport, 2001, v. 12 n. 3, p. 541-545en_US
dc.identifier.issn0959-4965en_US
dc.identifier.urihttp://hdl.handle.net/10722/149604-
dc.description.abstractFollowing ventral root avulsion in neonatal animals, the degeneration of spinal motoneurons occurs by an apoptotic-like morphological pathway. In adult animals, however, the mechanism of degeneration of injured motoneurons is still controversial. Because caspases are important mediators of apoptosis, we have investigated the effects of the caspase inhibitors, benzyloxycarbonyl-Asp(OMe)fluoromethylketone (Boc-D-FMK), and N-acetyl-Asp-Glu-Val-Asp aldehyde (Ac-DEVD-CHO) on the survival of neonatal and adult spinal motoneurons after root avulsion of the C7 spinal cord. In the control neonatal animals, virtually all motoneurons had degenerated by 7 days following root avulsion. Treatment with either 0.5 μg Boc-D-FMK or 1 μg Ac-DEVD-CHO enhanced the survival of motoneurons to 80% and 85% for up to 2 weeks post-injury. By 21 days post-injury, 70% of avulsed motoneurons were still present after Boc-D-FMK treatment, whereas all avulsed motoneurons died after treatment with Ac-DEVD-CHO. In adult animals, neither inhibitor was neuroprotective for motoneurons following root avulsion. In summary, the inhibition of caspases effectively rescued avulsed neonatal motoneurons which are died by apoptotic pathway. By contrast, because caspase inhibitors failed to rescue injured motoneurons in adult animals, their death may occur by a non-apoptotic pathway. © 2001 Lippincott Williams & Wilkins.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.neuroreport.comen_US
dc.relation.ispartofNeuroReporten_US
dc.subjectApoptosis-
dc.subjectCaspases-
dc.subjectNeuronal survival-
dc.subjectSpinal motoneurons-
dc.subject.meshAge Factorsen_US
dc.subject.meshAmino Acid Chloromethyl Ketones - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshAxotomyen_US
dc.subject.meshCaspases - Antagonists & Inhibitorsen_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshCysteine Proteinase Inhibitors - Pharmacologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshFemaleen_US
dc.subject.meshMotor Neurons - Cytology - Enzymologyen_US
dc.subject.meshOligopeptides - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSpinal Nerve Roots - Cytology - Injuries - Physiologyen_US
dc.titleCaspase inhibitors promote the survival of avulsed spinal motoneurons in neonatal ratsen_US
dc.typeArticleen_US
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_US
dc.identifier.emailYip, HK:hkfyip@hku.hken_US
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_US
dc.identifier.authorityWu, W=rp00419en_US
dc.identifier.authorityYip, HK=rp00285en_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00001756-200103050-00022-
dc.identifier.pmid11234760-
dc.identifier.scopuseid_2-s2.0-0035809758en_US
dc.identifier.hkuros74630-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035809758&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume12en_US
dc.identifier.issue3en_US
dc.identifier.spage541en_US
dc.identifier.epage545en_US
dc.identifier.isiWOS:000167069000022-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChan, YM=36989085800en_US
dc.identifier.scopusauthoridWu, W=7407081122en_US
dc.identifier.scopusauthoridYip, HK=7101980864en_US
dc.identifier.scopusauthoridSo, KF=34668391300en_US
dc.identifier.scopusauthoridOppenheim, RW=7102628195en_US
dc.identifier.issnl0959-4965-

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