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By P. H. Seeburg, R. Brusa, M. Higuchi, R. Sprengel (auth.), P. H. Seeburg, I. Bresink, L. Turski (eds.)

Ernst Schering examine starting place Workshop 23Excitatory Amino Acids: From Genes to Therapy Editors: P. Seeburg, I. Bresink, L. Turski during this booklet rising questions of present glutamate examine are addressed and new pathways which glutamate study may possibly absorb the longer term mentioned. because glutamate antagonists are nonetheless the most important wish for the remedy of neurodegenerative problems in people, examine actions committed in the direction of the advance of such novel medicines are the point of interest of public consciousness. The ebook reviews at the most up-to-date discoveries within the box of neuroprotection and neurodegeneration.

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1995) leads to enhanced vulnerability to agonist-induced cytotoxicity. Heterozygous transgenic mice engineered for a Q/R editing deficient GluR2 allele (Brusa et al. 1995) express AMPA receptors with increased Ca2+ permeability, particularly in hippocampal and neocortical principal neurons. The mice develop recurrent seizures and die within the first 3 weeks of life, with cell loss in the hippocampus. In these animals, unedited GluR2 may contribute to the formation of a greater number of Ca2+-permeable AMPA receptors than in the GluR2 knockout mice.

GluRl and GluR3 did not significantly change between 12-24 h, whereas GluR2 continued to decrease. At 24 h GluR2 is significantly different vs. GluRl and GluR3. B Hybridization levels in CA3. Modest decreases are observed for all probes. GluR2 is significantly different at 24 h vs. earlier time points but not vs. GluRl or GluR3. C Hybridization levels in dentate gyrus. None of the probes are significantly different from controls at any time point. Statistical analysis was performed on logit-transformed normalized percent optical densities by analysis of variance and Tukey's w-test for multiple comparisons.

1997). Parallel in situ hybridization indicated that GluR2 mRNA expression was markedly and specifically reduced in CAl pyramidal cells following global ischemia, but with a slower onset than in rats. Optical ratio imaging with the Ca2+ indicator dye fura-2 revealed that AMPA induced a transient but pronounced increase in intracellular free Ca2+ in individual CAl neurons 72 h after the ischemic insult, but not in controls. The AMPA receptor-mediated Ca2+ influx was blocked by CNQX; basal intracellular free Ca2+ concentrations did not differ in control and postischemic pyramidal cells.

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