| First Author | Row BW | Year | 2004 |
| Journal | J Neurochem | Volume | 89 |
| Issue | 1 | Pages | 189-96 |
| PubMed ID | 15030403 | Mgi Jnum | J:90580 |
| Mgi Id | MGI:3044249 | Doi | 10.1111/j.1471-4159.2004.02352.x |
| Citation | Row BW, et al. (2004) Platelet-activating factor receptor-deficient mice are protected from experimental sleep apnea-induced learning deficits. J Neurochem 89(1):189-96 |
| abstractText | 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. |
