Impact of Actin Filament Stabilization on Adult Hippocampal and Olfactory Bulb Neurogenesis

• DOI: 10.1523/jneurosci.4231-09.2010
• Publication Date: 2010-03-04T16:06:35Z
• Authors: Golo Kronenberg; Karen Gertz; Tina Baldinger; Imke Kirste; Sarah Eckart; Ferah Yildirim; Shengbo Ji; Isabella Heuser; Helmut Schröck; Heide Hörtnagl; Reinhard Sohr; Pierre Chryso Djo...; René Jüttner; Rainer Glass; Ingo Przesdzing; Jitender Kumar; Dorette Freyer; Rainer Hellweg; Helmut Kettenmann; Klaus Benno Fink; Matthias Endres
• Keywords: Gelsolin; Rostral migratory stream; Neuroblast

Rearrangement of the actin cytoskeleton is essential for dynamic cellular processes. Decreased turnover and rigidity cytoskeletal structures have been associated with aging cell death. Gelsolin a Ca 2+ -activated actin-severing protein that widely expressed throughout adult mammalian brain. Here, we used gelsolin-deficient ( Gsn −/− ) mice as model system filament stabilization. In mice, emigration newly generated cells from subventricular zone into olfactory bulb was slowed. vitro , gelsolin deficiency did not affect proliferation or neuronal differentiation neural progenitors (NPCs) but resulted in retarded migration. Surprisingly, hippocampal neurogenesis robustly induced by deficiency. The ability NPCs to intrinsically sense excitatory activity thereby implement coupling between network has recently established. Depolarization-induced [Ca ] i increases exocytotic neurotransmitter release were enhanced synaptosomes. Importantly, treatment synaptosomes mycotoxin cytochalasin D, which, like gelsolin, produces disassembly, decreased influx subsequent norepinephrine wild-type levels. Similarly, depolarization-induced glutamate brain slices increased. Furthermore, increased special microenvironment characterized density perfused vessels, regional cerebral blood flow, endothelial nitric oxide synthase (NOS-III) expression hippocampus. Together, reduced filamentous presynaptic terminals causes and, subsequently, elevated acting on progenitors. Increased hippocampus vascular niche neurogenesis.