1. An Anti-Apoptotic Action of Glia Lipoproteins
Hideki Hayashi, Robert B. Campenot, Dennis E. Vance, and Jean E. Vance
Apolipoprotein E (apoE), an apolipoprotein contained in lipoproteins secreted by CNS glia, is perhaps best known because its 4 allele is a risk factor for late-onset Alzheimer's disease. This week, Hayashi et al. outline a signaling pathway by which these apoE-containing lipoproteins can inhibit apoptosis. The authors induced apoptosis in cultured rat retinal ganglion cells by removing trophic factors from the media. Glia-conditioned media or glia-secreted lipoproteins protected neurons from apoptosis. Protection specifically required apoE and was blocked either by receptor-associate protein, which competes with ligands of low-density lipoprotein receptors (LDLrs), or by inhibition of the apoE receptor LDLr-related protein (LRP). Downstream of LRP, signaling involved protein kinase C, possibly by phosphorylating and inactivating the proapoptotic glycogen synthase kinase-3. ApoE3 was more effective in preventing apoptosis than apoE4.
2. Myelination and Remyelination in the Pregnant Mouse
Christopher Gregg, Viktor Shikar, Peter Larsen, Gloria Mak, Andrew Chojnacki, V. Wee Yong, and Samuel Weiss
This week, Gregg et al. report that pregnancy in rats increased myelin-forming oligodendrocytes and myelin formation, an effect the authors attribute to prolactin. In corpus callosum and spinal cord, oligodendrocyte precursor cells (OPCs) increased in early pregnancy, followed by an increase in oligodendrocytes. Postpartum, pregnancy-generated oligodendrocytes extended processes. There was also an associated increase in myelination of callosal axons. To test the effects of pregnancy on the repair of demyelinating lesions, the authors injected lysolecithin into the spinal cord. Pregnant rats displayed smaller lesions, fewer demyelinated axons, and more remyelinated axons. The prolactin (PRL) receptor, expresse
Contact: Sara Harris
Society for Neuroscience