Reelin and mDab1 regulate the development of hippocampal connections

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

“…These data complement previous findings obtained from cultured hippocampal neurons that revealed the dependence of the somatic NMDA receptor composition, trafficking, assembly, and maintenance on Reelin-mediated signaling (Sinagra et al, 2005;Groc et al, 2007;Campo et al, 2009). They also fit with in situ observations where neurons exhibit reduced axonal (Del Rio et al, 1997;Borrell et al, 1999) and dendritic branching, as well as stunted dendritic growth and significantly fewer spines in the complete or partial absence of Reelin or its receptors Niu et al, 2004;Borrell et al, 2007;Qiu and Weeber, 2007;Niu et al, 2008). This likely underlies the impaired performance of heterozygous reeler mice in certain learning and memory tasks as compared to wild type controls (Tueting et al, 1999;Krueger et al, 2006;Qiu et al, 2006c;Qiu et al, 2006a;Barr et al, 2007;Qiu and Weeber, 2007).…”

“…Reelin-induced augmentation of Ca 2+ entry through NMDA receptors is likely also involved in the regulation of downstream signaling cascades involved in learning and memory . These data fit with the observations that in the absence of Reelin or the Reelin receptors, neurons exhibit stunted dendritic growth, a reduction in dendritic branches and significantly fewer spines (Del Rio et al, 1997;Borrell et al, 1999;Trommsdorff et al, 1999;Niu et al, 2004;Borrell et al, 2007;Qiu and Weeber, 2007;Niu et al, 2008). …”

Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease

“…Numerous independent studies and observations point toward a role for Reelin and ApoE receptors in the formation of neuronal connections (Del Rio et al 1997;Borrell et al 2007) and the generation of dendritic complexity Costa et al 2001;Niu et al 2004;Matsuki et al 2008;Hoe et al 2009). The latter may, however, not be entirely dependent on Apoer2 and Vldlr (Chameau et al 2009) and may also involve interactions with APP (Hoe et al 2009).…”

The tumor suppressor Nf2 regulates corpus callosum development by inhibiting the transcriptional coactivator Yap

“…Lineage-tracing experiments are required to determine whether this is the case. Intriguingly, these guidepost neurons share several features with Cajal-Retzius cells: both express Calretinin but are glutamatergic, whereas most if not all other cortical Calretinin + neurons are GABAergic; both exist transiently during development and both guide axonal navigation (Borrell et al, 2007;Del Rio et al, 1997). A source of Cajal-Retzius cells is the cortical hem, residing along the caudal telencephalic midline immediately posterior to the GW (Grove et al, 1998).…”