کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3065027 | 1580467 | 2009 | 8 صفحه PDF | دانلود رایگان |
The area postrema (AP) represents the medullary sensory circumventricular organ lacking endothelial blood–brain barrier function at the base of the 4th cerebral ventricle. Administration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) or the nitric oxide (NO) donor diethylamino-diazenolate-2-oxide (DEA) caused fast transient rises in intracellular calcium concentrations ([Ca2+]i) in distinct populations of cells investigated in a primary microculture of the rat AP. TNF-α caused rapid elevations of [Ca2+]i in 8% of all neurons and astrocytes investigated, with limited responses of microglial cells and no responses of oligodendrocytes. 15% of all neurons investigated responded to IL-1β, while only 5–7% of the other cell types showed rises in [Ca2+]i. The most pronounced effects were caused by treatment with DEA with some 20% responsive astrocytes and oligodendrocytes, 15% neurons and 10% microglial cells. Evidently, the AP can act as a sensor for circulating TNF-α and IL-1β, or for locally produced cytokines and NO during infection and inflammation.
Journal: Journal of Neuroimmunology - Volume 206, Issues 1–2, 3 January 2009, Pages 44–51