[PDF][PDF] Coordinated interaction of neurogenesis and angiogenesis in the adult songbird brain
A Louissaint, S Rao, C Leventhal, SA Goldman - Neuron, 2002 - cell.com
A Louissaint, S Rao, C Leventhal, SA Goldman
Neuron, 2002•cell.comNeurogenesis proceeds throughout life in the higher vocal center (HVC) of the adult
songbird neostriatum. Testosterone induces neuronal addition and endothelial division in
HVC. We asked if testosterone-induced angiogenesis might contribute importantly to HVC
neuronal recruitment. Testosterone upregulated both VEGF and its endothelial receptor,
VEGF-R2/Quek1/KDR, in HVC. This yielded a burst in local HVC angiogenesis. FACS-
isolated HVC endothelial cells produced BDNF in a testosterone-dependent manner. In vivo …
songbird neostriatum. Testosterone induces neuronal addition and endothelial division in
HVC. We asked if testosterone-induced angiogenesis might contribute importantly to HVC
neuronal recruitment. Testosterone upregulated both VEGF and its endothelial receptor,
VEGF-R2/Quek1/KDR, in HVC. This yielded a burst in local HVC angiogenesis. FACS-
isolated HVC endothelial cells produced BDNF in a testosterone-dependent manner. In vivo …
Abstract
Neurogenesis proceeds throughout life in the higher vocal center (HVC) of the adult songbird neostriatum. Testosterone induces neuronal addition and endothelial division in HVC. We asked if testosterone-induced angiogenesis might contribute importantly to HVC neuronal recruitment. Testosterone upregulated both VEGF and its endothelial receptor, VEGF-R2/Quek1/KDR, in HVC. This yielded a burst in local HVC angiogenesis. FACS-isolated HVC endothelial cells produced BDNF in a testosterone-dependent manner. In vivo, HVC BDNF rose by the third week after testosterone, lagging by over a week the rise in VEGF and VEGF-R2. In situ hybridization revealed that much of this induced BDNF mRNA was endothelial. In vivo, both angiogenesis and neuronal addition to HVC were substantially diminished by inhibition of VEGF-R2 tyrosine kinase. These findings suggest a causal interaction between testosterone-induced angiogenesis and neurogenesis in the adult forebrain.
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