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GluN2B ser1303

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https://www.readbyqxmd.com/read/22929440/%C3%AE-camkii-is-differentially-regulated-in-brain-regions-that-exhibit-differing-sensitivities-to-ischemia-and-excitotoxicity
#1
Kathryn A Skelding, Neil J Spratt, Lisa Fluechter, Phillip W Dickson, John A P Rostas
Different brain regions exhibit differing sensitivities to ischemia/excitotoxicity. Whether these differences are due to perfusion or intrinsic factors has not been established. Herein, we found no apparent association between sensitivity to ischemia/excitotoxicity and the level of expression or basal phosphorylation of calcium/calmodulin-stimulated protein kinase II (αCaMKII) or glutamate receptors. However, we demonstrated significant differences in CaMKII-mediated responses after ischemia/excitotoxic stimulation in striatum and cortex...
December 2012: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/18657555/antidepressants-reverse-the-attenuation-of-the-neurotrophic-mek-mapk-cascade-in-frontal-cortex-by-elevated-platform-stress-reversal-of-effects-on-ltp-is-associated-with-glua1-phosphorylation
#2
Hongshi Qi, François Mailliet, Michael Spedding, Cyril Rocher, Xiaoqun Zhang, Philippe Delagrange, Bruce McEwen, Thérèse M Jay, Per Svenningsson
Exposure to stress causes dysfunctions in circuits connecting hippocampus and prefrontal cortex (H-PFC). Long term potentiation (LTP) induced in vivo in rats at H-PFC synapses is impaired by acute elevated platform stress in a manner that can be restored by treatment with certain antidepressants. To identify biochemical pathways in rat frontal cortex underlying this stress-mediated impairment of synaptic plasticity, we examined the phosphorylation state of receptors, signaling proteins and transcription factors implicated in neuronal plasticity...
January 2009: Neuropharmacology
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