Figure 2.

Opposite roles of EGFR-dependent signalling and TGFβ-dependent signalling in the age-associated decline of SVZ neurogenesis. (A) In SVZ NSPCs, TGFα promotes neurogenesis by activating EGFR and increasing the levels of phosphorylated ERK (pERK). In contrast, TGFβ1 hampers neurogenesis by activating TGFβ receptors and enhancing the levels of phosphorylated Smad3 (pSmad3). (B) In NSPCs of the young adult SVZ, ERK activation predominates over Smad3 activation and the neurogenic process is efficiently stimulated. During aging, the relative ratio of ERK and Smad3 activation is reversed, leading to a decline in neurogenesis. See text for further details. EGFR indicates epidermal growth factor receptor; TGF, transforming growth factor.