期刊
JOURNAL OF NEUROCHEMISTRY
卷 89, 期 1, 页码 189-196出版社
WILEY
DOI: 10.1111/j.1471-4159.2004.02352.x
关键词
apoptosis; inflammation; intermittent hypoxia; platelet-activating factor; sleep-disordered breathing; spatial learning
资金
- NHLBI NIH HHS [HL63912, HL69932, HL66385] Funding Source: Medline
- NICHD NIH HHS [F32 HD 42396] Funding Source: Medline
Intermittent hypoxia (IH) during sleep, a hallmark of sleep apnea, is associated with neurobehavioral impairments, regional neurodegeneration and increased oxidative stress and inflammation in rodents. Platelet-activating factor (PAF) is an important mediator of both normal neural plasticity and brain injury. We report that mice deficient in the cell surface receptor for PAF (PAFR-/-), a bioactive mediator of oxidative stress and inflammation, are protected from the spatial reference learning deficits associated with IH. Furthermore, PAFR-/- exhibit attenuated elevations in inflammatory signaling (cyclo-oxygenase-2 and inducible nitric oxide synthase activities), degradation of the ubiquitin-proteasome pathway and apoptosis observed in wild-type littermates (PAFR+/+) exposed to IH. Collectively, these findings indicate that inflammatory signaling and neurobehavioral impairments induced by IH are mediated through PAF receptors.
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