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Figure 8 | BMC Neuroscience

Figure 8

From: Hyperosmotic stimulus induces reversible angiogenesis within the hypothalamic magnocellular nuclei of the adult rat: a potential role for neuronal vascular endothelial growth factor

Figure 8

Dexamethasone inhibits both VEGF expression and SON proliferative response. Untreated (A-B) or Dexamethasone treated (C-F) rats were osmotically stimulated during 6 days and injected with BrdU 5 hours before their fixation. Stack confocal images (10 μm-thick) of sections double immunostained for VEGF and BrdU (A-D). As compared with the control rat (A-B), the SON of the dexamethasone treated rat exhibits decreased immunostaining for VEGF (C) and a complete disappearance of BrdU-labeled nuclei (D). By contrast, dexamethasone treatment has no effect on the BrdU-labeling of proliferative cells within the subventricular zone of the lateral ventricle (insets). Note that in the control rat, BrdU-labeled nuclei are essentially localized to the core of the SON that contains the VEGF-labeled neurons, and are scarce in the ventral portion of the nucleus that contains labeled astrocytes (stars in A and B). BrdU: bromodeoxyuridine; EBA: endothelial brain antigen; SON: supraoptic nucleus; VEGF: vascular endothelial growth factor. Scale bar: A-D = 100 μm.

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