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Vol. 16, Issue 1, 339-347, January 2005

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NGF Controls Dendrite Development in Hippocampal Neurons by Binding to p75^NTR and Modulating the Cellular Targets of Notch

Patricia Salama-Cohen ^* , María-Ángeles Arévalo ^* , Jochen Meier , Rosemarie Grantyn , and Alfredo Rodríguez-Tébar ^* 

^* Instituto Cajal de Neurobiología, Consejo Superior de Investigaciones Científicas, E28002 Madrid, Spain; Johannes Mueller Institute for Physiology, Medical Faculty (Charité) of the Humboldt University Berlin, D-10117 Berlin, Germany

Submitted May 31, 2004; Revised October 6, 2004; Accepted October 8, 2004
Monitoring Editor: Pamela Silver

Notch and neurotrophins control neuronal shape, but it is not known whether their signaling pathways intersect. Here we report results from hippocampal neuronal cultures that are in support of this possibility. We found that low cell density or blockade of Notch signaling by a soluble Delta-Fc ligand decreased the mRNA levels of the nuclear targets of Notch, the homologues of enhancer-of-split 1 and 5 (Hes1/5). This effect was associated with enhanced sprouting of new dendrites or dendrite branches. In contrast, high cell density or exposure of low-density cultures to NGF increased the Hes1/5 mRNA, reduced the number of primary dendrites and promoted dendrite elongation. The NGF effects on both Hes1/5 expression and dendrite morphology were prevented by p75-antibody (a p75^NTR-blocking antibody) or transfection with enhancer-of-split 6 (Hes6), a condition known to suppress Hes activity. Nuclear translocation of NF-kappaB was identified as a link between p75^NTR and Hes1/5 because it was required for the up-regulation of these two genes. The convergence of the Notch and p75^NTR signaling pathways at the level of Hes1/5 illuminates an unexpected mechanism through which a diffusible factor (NGF) could regulate dendrite growth when cell-cell interaction via Notch is not in action.

These authors contributed equally to this work.

Corresponding author. E-mail address: rodriguez{at}cajal.csic.es.

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