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Conference Paper: Neuropeptide Y and its receptor analogs modulate ischemia-induced nitric oxide production

TitleNeuropeptide Y and its receptor analogs modulate ischemia-induced nitric oxide production
Authors
KeywordsMCAO
NITRIC OXIDE
NPY
Issue Date2001
PublisherSociety for Neuroscience. The Journal's web site is located at http://sfn.scholarone.com/
Citation
Neuroscience 2001, San Diego, CA, 10-15 November 2001, Presentation no. 328.16 How to Cite?
AbstractWe previously showed that intracerebroventricular (ICV) injection of neuropeptide Y (NPY) or Y1 agonist increased the infarct volume whereas administration of BIBP3226, a NPY Y1 antagonist, reduced the infarct volume. Nitric oxide (NO) is a mediator of ischemic damage. In this study, we examined the effects of NPY and its receptor analogs on NO production during middle cerebral artery occlusion. Male Sprague-Dawley rats were anesthetized with sodium pentobarbital. NPY (10 mcg/kg), [Leu31, Pro34]-NPY (30 mcg/kg), BIBP3226 (15 mcg/kg), NPY3-36 (15 mcg/kg) or vehicle was administered via a slow ICV injection at 2 minutes after onset of ischemia. NO measurement was made in the brain slices between Bregma levels +2 and –4 mm. NO trapping reagents, diethyldithiocarbamate and iron citrate, were administered via intraperitoneal and subcutaneous injection, respectively, at 15 minutes prior to ischemia. Tissue NO concentration was measured using electron paramagnetic resonance spectroscopy. Results from the ischemic side were expressed as a percentage of the non-ischemic side and compared among groups using two-tailed Student’s t test. After 15 minutes of focal cerebral ischemia, the relative NO concentration increased to 131.9±8.0% (mean±SEM; n=8). NPY treatment further increased the NO signal (250.9±50.5%; n=8, P<0.05), whereas BIBP3226 reduced the NO signal (69.6±8.8%; n=8, P<0.05). Treatment with [Leu31, Pro34]-NPY and NPY3-36 did not affect the ischemia-induced NO signal (133.4±13.3%, n=8; 129.2±21.8%, n=8). Thus, exogenous NPY and its receptor analogs may affect the infarct volume via their effects on ischemic-induced NO generation.
Persistent Identifierhttp://hdl.handle.net/10722/54147

 

DC FieldValueLanguage
dc.contributor.authorChen, SHen_HK
dc.contributor.authorCheung, RTFen_HK
dc.date.accessioned2009-04-03T07:37:58Z-
dc.date.available2009-04-03T07:37:58Z-
dc.date.issued2001en_HK
dc.identifier.citationNeuroscience 2001, San Diego, CA, 10-15 November 2001, Presentation no. 328.16en_HK
dc.identifier.urihttp://hdl.handle.net/10722/54147-
dc.description.abstractWe previously showed that intracerebroventricular (ICV) injection of neuropeptide Y (NPY) or Y1 agonist increased the infarct volume whereas administration of BIBP3226, a NPY Y1 antagonist, reduced the infarct volume. Nitric oxide (NO) is a mediator of ischemic damage. In this study, we examined the effects of NPY and its receptor analogs on NO production during middle cerebral artery occlusion. Male Sprague-Dawley rats were anesthetized with sodium pentobarbital. NPY (10 mcg/kg), [Leu31, Pro34]-NPY (30 mcg/kg), BIBP3226 (15 mcg/kg), NPY3-36 (15 mcg/kg) or vehicle was administered via a slow ICV injection at 2 minutes after onset of ischemia. NO measurement was made in the brain slices between Bregma levels +2 and –4 mm. NO trapping reagents, diethyldithiocarbamate and iron citrate, were administered via intraperitoneal and subcutaneous injection, respectively, at 15 minutes prior to ischemia. Tissue NO concentration was measured using electron paramagnetic resonance spectroscopy. Results from the ischemic side were expressed as a percentage of the non-ischemic side and compared among groups using two-tailed Student’s t test. After 15 minutes of focal cerebral ischemia, the relative NO concentration increased to 131.9±8.0% (mean±SEM; n=8). NPY treatment further increased the NO signal (250.9±50.5%; n=8, P<0.05), whereas BIBP3226 reduced the NO signal (69.6±8.8%; n=8, P<0.05). Treatment with [Leu31, Pro34]-NPY and NPY3-36 did not affect the ischemia-induced NO signal (133.4±13.3%, n=8; 129.2±21.8%, n=8). Thus, exogenous NPY and its receptor analogs may affect the infarct volume via their effects on ischemic-induced NO generation.-
dc.languageengen_HK
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://sfn.scholarone.com/en_HK
dc.relation.ispartofSociety for Neuroscience Annual Meeting-
dc.rightsSociety for Neuroscience Abstract viewer & itinerary planner. Copyright © Society for Neuroscience.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectMCAO-
dc.subjectNITRIC OXIDE-
dc.subjectNPY-
dc.titleNeuropeptide Y and its receptor analogs modulate ischemia-induced nitric oxide productionen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailCheung, RTF: rtcheung@hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.hkuros115200-

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