作者: Neeraja Sammeta , Timothy S. McClintock
DOI: 10.1002/CNE.22305
关键词:
摘要: More than any other neuron, olfactory sensory neurons are exposed to environmental insults. Surprisingly, their only documented response damaging stress is apoptosis and subsequent replacement by new neurons. However, they expressed unfolded protein genes, a transcriptionally regulated defense mechanism activated many types of The transcripts Xbp1, spliced Chop (Ddit3), BiP (Hspa5) were decreased when external access stressors was reduced blocking nostril (naris occlusion). These Nrf2 (Nfe2l2) increased systemic application tunicamycin or the selective olfactotoxic chemical methimazole. Methimazole's effects overcame naris occlusion, independent odor-evoked neuronal activity. Chemical therefore major chronic activator in Stress-dependent repression antiapoptotic gene Bcl2 absent, however, suggesting for disconnecting UPR from tolerating response. Environmental also affect both sustentacular cells that support respiratory epithelia, because occlusion expression xenobiotic transformation enzyme Cyp2a5 cells, methimazole altered abundance antibacterial lectin Reg3g epithelia.