g., prior learning experience, memory expression prior to deficit). The following experiments examined the size and persistence of these deficits after matching both the amount of experience with MDV3100 in vivo a context and the levels of performance in that context prior to delivery of the protein synthesis inhibitor anisomycin. We found that systemic or intrahippocampal administration of anisomycin caused a deficit in groups receiving context conditioning (consolidation groups) or reactivation (reconsolidation groups) immediately prior to the injections. With systemic injections, the deficit was larger and more persistent in consolidation groups;

with intrahippocampal injections, the initial deficit was statistically identical, yet was more persistent in the consolidation group. These experiments showed that when experiences and performance are matched prior to anisomycin injections, consolidation deficits are generally larger and more persistent compared to reconsolidation deficits.”
“Glaucoma, one of the leading causes of irreversible blindness, is characterized by progressive degeneration of retinal ganglion cells (RGCs)

and optic nerves. Although glaucoma is often associated with elevated intraocular pressure, recent studies have shown a relatively high prevalence of normal tension glaucoma (NTG) in glaucoma patient GSK1120212 cost eltoprazine populations In the mammalian retina, glutamate/aspartate transporter (GLAST) is localized to Muller glial cells. whereas excitatory amino acid carrier 1 (EAAC1) is expressed in neural cells, including RGCs. Since the loss of GLAST or EAAC1 leads to retinal degeneration similar to that seen in NTG, we examined the effects of interleukin-1 (IL-1) on RGC death in GLAST- and EAAC1-deficient mice. IL-1 promoted increased glutamate uptake in Muller

cells by suppressing intracellular Na(+) accumulation, which is necessary to counteract Na(+)-glutamate cotransport The observed trends for the glutamate uptake increase in the wild-type (WT), GLAST- and EAAC1-deficient mice were similar: however, the baseline glutamate uptake and intracellular Na(+) concentration in the GLAST-deficient mice were significantly lower than those in the wild-type mice. Consistently, pretreatment with IL-1 exhibited no beneficial effects on glutamate-induced RGC degeneration in the GLAST-deficient mice. In contrast, IL-1 significantly increased glutamate uptake by Muller cells and the number of surviving RGCs in the wild-type and EAAC1-deficient mice. Our findings suggest that the use of IL-1 for enhancing the function of glutamate transporters may be useful for neuroprotection in retinal degenerative disorders including NTG. (c) 2009 Elsevier Ireland Ltd All rights reserved.