Tumor necrosis factor-α, interleukin-1β and nitric oxide induce calcium transients in distinct populations of cells cultured from the rat area postrema

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.