Premium
Enrichment environment exposure induces proliferation of doublecortin‐expressing immature neurons in layer II across the young adult guinea pig frontal cortex
Author(s) -
Charles-Felix Calvo,
Jean-Léon Thomas,
Kun Xiong,
Chunling Fan,
Mengqi Zhang,
Zhi Li,
Zhengyu,
Yang,
Lei Shang,
Jufang Huang
Publication year - 2012
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2012.03.310
Subject(s) - doublecortin , neurogenesis , neuroscience , cortex (anatomy) , biology , frontal cortex , environmental enrichment , psychology , hippocampus , dentate gyrus
In the adult mammalian brain, the potential to generate new neurons is restricted to a limited number of sites called neurogenic niches, which are localized in the subventricular zone (SVZ) lining the cerebral ventricles and in the dentate gyrus (DG) of the hippocampus. Injury of brain tissue resulting from trauma or pathologies activates neurogenesis in these niches, attesting to an endogenous repair potential that is generally not sufficient to allow a complete rescue. To enhance this endogenous neurogenic response without negative side effects, it is crucial to characterize the mechanisms which are active in neurogenic niches. Functionally, members of the vascular endothelial growth factor (VEGF) family stimulate adult neurogenesis and neuronal plasticity, opening potential approaches for repair of neurodegenerative diseases. However, it has been unclear whether VEGFs stimulate neurogenesis directly via VEGF receptors (VEGFRs) expressed by neural cells, or indirectly via the release of growth factors from angiogenic capillaries. We have reported that the lymphangiogenic growth factor VEGF-C is expressed by neural cells and provides trophic support to neural progenitor cells during brain development (Le Bras, Nature Neurosci, 2006). We have also shown that its receptor, VEGFR-3, is expressed by adult SVZ astrocytes including NSCs, and is critical for adult neurogenesis by acting directly in astrocytes, but not endothelial cells (Calvo, Genes & Dev, 2011). Therefore, VEGFC/VEGFR-3 signaling is a new regulator of neurogenesis in the adult subventricular zone. We have now extended these pioneer studies to the other main neurogenic niche of the murine adult brain, the hippocampus, to investigate the physiological importance of VEGFC/VEGFR-3 signaling in neurogenesis, and to carry out a mechanistic study of the cellular and molecular responses of VEGFR-3 neural cells to VEGF-C. We will present our more recent findings on these processes.