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pubmed-article:11223654pubmed:abstractTextGasping is an important mechanism for survival that appears to be developmentally modulated by the glutamate-nitric oxide (NO) pathway. However, the temporal characteristics of NO brain tissue levels during gasping are unknown. We hypothesized that during anoxia-induced gasping, the gasping frequency would be closely correlated with caudal brainstem tissue NO concentrations in developing rats. Brainstem and cortical tissue NO levels were measured during anoxia using a voltammetric electrode in adult rats and 5-day-old pups during control conditions and following pretreatment with the NMDA receptor antagonist MK-801 (1 mg/kg) or the neuronal NO synthase inhibitor 7-nitro-indazole (7-NI; 100 mg/kg). In young animals, NO tissue levels followed a triphasic trajectory coincident with gasp frequency which was markedly altered by MK-801 and 7-NI, albeit with preservation of gasp frequency-NO tissue level relationships. In adult rats, 40-fold higher NO tissue levels occurred and followed a monophasic trajectory coincident with gasp patterning. In the cortex, monophasic increases in NO levels occurred at all ages. We conclude that anoxia-induced gasping neurogenesis is modulated via NMDA-NO mechanisms in the developing rat. We postulate that higher NO brainstem concentrations may favor early autoresuscitation, but limit anoxic tolerance.lld:pubmed
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pubmed-article:11223654pubmed:authorpubmed-author:TorresJ EJElld:pubmed
pubmed-article:11223654pubmed:authorpubmed-author:GreenG SGSlld:pubmed
pubmed-article:11223654pubmed:copyrightInfoCopyright 2001 S. Karger AG, Basellld:pubmed
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pubmed-article:11223654pubmed:volume79lld:pubmed
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pubmed-article:11223654pubmed:pagination122-30lld:pubmed
pubmed-article:11223654pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:11223654pubmed:year2001lld:pubmed
pubmed-article:11223654pubmed:articleTitleBrainstem nitric oxide tissue levels correlate with anoxia-induced gasping activity in the developing rat.lld:pubmed
pubmed-article:11223654pubmed:affiliationKosair Children's Hospital Research Institute, Departments of Pediatrics, Pharmacology and Toxicology, University of Louisville School of Medicine, KY 40202, USA. d0goza01@gwise.louisville.edulld:pubmed
pubmed-article:11223654pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11223654pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
pubmed-article:11223654pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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