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      Mice with experimental antiphospholipid syndrome display hippocampal dysfunction and a reduction of dendritic complexity in hippocampal CA1 neurones : Reduced dendritic complexity in eAPS mice

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          Most cited references31

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          The pathogenesis of the antiphospholipid syndrome.

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            A dual role for interleukin-1 in hippocampal-dependent memory processes.

            Ample research demonstrates that pathophysiological levels of the pro-inflammatory cytokine interleukin-1 (IL-1) produces detrimental effects on memory functioning. However, recent evidence suggests that IL-1 may be required for the normal physiological regulation of hippocampal-dependent memory. To substantiate the physiological role of IL-1 in learning and memory we examined the induction of IL-1 gene expression following a learning experience, and the effects of IL-1 signaling blockade, by either genetic or pharmacological manipulations, on memory functioning. We show that IL-1 gene expression is induced in the hippocampus 24h following fear-conditioning in wild type mice, but not in two mouse strains with impaired IL-1 signaling. Moreover, we report that mice with transgenic over-expression of IL-1 receptor antagonist restricted to the CNS (IL-1raTG) display impaired hippocampal-dependent and intact hippocampal-independent memory in the water maze and fear-conditioning paradigms. We further demonstrate that continuous administration of IL-1ra via osmotic minipumps during prenatal development disrupt memory performance in adult mice, suggesting that IL-1 plays a critical role not only in the formation of hippocampal-dependent memory but also in normal hippocampal development. Finally, we tested the dual role of IL-1 in memory by intracerebroventricular (ICV) administration of different doses of IL-1beta and IL-1ra following learning, providing the first systematic evidence that the involvement of IL-1 in hippocampal-dependent memory follows an inverted U-shaped pattern, i.e., a slight increase in brain IL-1 levels can improve memory, whereas any deviation from the physiological range, either by excess elevation in IL-1 levels or by blockade of IL-1 signaling, results in impaired memory.
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              A method for vibratome sectioning of Golgi-Cox stained whole rat brain.

              A method for impregnating the whole rat brain with Golgi-Cox stain and sectioning with the vibratome is described. The method is simple, inexpensive and provides good resolution of dendrites and spines.
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                Author and article information

                Journal
                Neuropathology and Applied Neurobiology
                Neuropathol Appl Neurobiol
                Wiley
                03051846
                August 2015
                August 2015
                April 30 2015
                : 41
                : 5
                : 657-671
                Affiliations
                [1 ]Department of Neuropathology; University Medical Center of the Johannes Gutenberg University Mainz; Mainz Germany
                [2 ]Department of Neurology; Chaim Sheba Medical Center; Sackler Faculty of Medicine; Tel Aviv University; Tel Hashomer Israel
                [3 ]Sagol School of Neuroscience; Tel Aviv University; Tel Aviv Israel
                [4 ]Focus Program Translational Neurosciences (FTN); Rhine Main Neuroscience Network (rmn 2 ); Germany
                Article
                10.1111/nan.12180
                0f3f0111-ab02-47bf-b5f5-c8399b1ce335
                © 2015

                http://doi.wiley.com/10.1002/tdm_license_1.1

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