Articles with the keyword: 


Prion protein attenuates excitotoxicity by inhibiting NMDA receptors
sea-maid submitted, created time 6 months 3 weeks (www.jcb.org)
To determine the physiological role of PrPC, this author examines the neurophysiological properties of hippocampal neurons isolated from PrP-null mice. 
Prions are usefull for disease
sea-maid submitted, created time 8 months 1 week (www.jcb.org)
The results of recent investigatoins suggest that normal prions might exert their protective effect on neurons by switching off a particular subset of NMDA receptors that contain a subunit called NR2D. The work also suggests a mechanism for the brain damage caused by prion diseases. Malformed prions coax normal molecules to misfold. As the amount of normal protein falls, neurons lose their protectors and become more vulnerable to death by overstimulation. 


annatto submitted, created time 1 year 7 months (mcb.asm.org)
"Synaptic scaffolding molecule (S-SCAM) interacts with a wide variety of molecules at excitatory and inhibitory synapses. It comprises three alternative splicing variants, S-SCAM{alpha}, -ß, and -{gamma}. We generated mutant mice lacking specifically S-SCAM{alpha}. S-SCAM{alpha}-deficient mice breathe and feed normally but die within 24 h after birth. Primary cultured hippocampal neurons from mutant mice have abnormally elongated dendritic spines. Exogenously expressed S-SCAM{alpha} corrects this abnormal morphology, while S-SCAMß and -{gamma} have no effect 


matrix submitted, created time 1 year 10 months (www.neuron.org)
NMDA receptors promote neuronal survival but also cause cell degeneration and neuron loss. Whole-genome expression profiling revealed that NMDA receptor signaling is decoded at the genomic level through activation of two distinct, largely nonoverlapping gene-expression programs. These results help explain the opposing roles of synaptic and extrasynaptic NMDA receptors on neuronal fate. very cool application of whole-genome expression profiling. 
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