Box 345, University of Colorado Boulder, Boulder, CO 80309-0345. E-mail: ruth.barrientos: Unterschied zwischen den Versionen

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Even though HFD consumption alone has been shown to induce proinflammatory gene expression in numerous brain regions, such as hippocampus (Hansen et al., 1998; Thaler et al., 2012; Beilharz et al., 2014, 2016), it needs to be noted that these research especially incorporated a substantial sugar element in their high-fat diet regimen, which could be a crucial factor. A bigger physique of literature (from studies employing saturated HFDs that usually do not have higher sugar contents, which include the present a single), suggests that hippocampal cells are primed by HFD consumption, and that a secondary challenge will have to happen prior to neuroinflammatory cytokines are detected or memory impairments are observed (Boitard et al., 2014; Cai et al., 2014; Knight et al., 2014; Sobesky et al., 2014). These research have shown that HFD consumption alone does not create elevated cytokine expression inside the brain, but does elevate microglial markers of activation. Moreover, shortterm HFD consumption sensitizes the hypothalamus and hippocampus to over-respond to an immune challenge, for instance to lipopolysaccharide (LPS), and, in turn, produces functional impairments mediated by those brain regions. Even so, little is recognized in regards to the mechanisms that mediate this short-term HFD-induced priming impact, and thus could be the focus of your present study. Here, we explored the novel idea that short-term consumption of HFD would induce an elevation in hippocampal corticosterone (CORT), which would in turn prime the hippocampus to amplify its inflammatory response to a mild inflammatory challenge, finally resulting in impairments in memory consolidation. Despite its classic function as an immunosuppressant, there's a growing literature demonstrating that CORT can prime hippocampal microglia (Frank et al., 2010a, 2014; CYT387 web Barrientos et al., 2015a) and potentiate the neuroinflammatory response to a subsequent inflammatory challenge (Frank et al., 2010a; Munhoz et al., 2010; Hains et al., 2011; Loram et al., 2011).Box 345, University of Colorado Boulder, Boulder, CO 80309-0345. E-mail: ruth.barrientos@colorado.edu. DOI:http://dx.doi.org/10.1523/ENEURO.0113-16.2016 Copyright ?2016 Sobesky et al. This can be an open-access report distributed below the terms of your Inventive Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium offered that the original work is correctly attributed.a proinflammatory response there and causing behavioral modifications (Milanski et al., 2009; Maric et al., 2014). Nevertheless, for factors that stay unclear, absolutely free fatty acids do not pass directly into the hippocampus (Milanski et al., 2009). Though HFD consumption alone has been shown to induce proinflammatory gene expression in different brain regions, including hippocampus (Hansen et al., 1998; Thaler et al., 2012; Beilharz et al., 2014, 2016), it needs to be noted that these research specifically integrated a substantial sugar element in their high-fat diet program regimen, which may be a important issue. A bigger body of literature (from research employing saturated HFDs that usually do not have high sugar contents, for instance the present a single), suggests that hippocampal cells are primed by HFD consumption, and that a secondary challenge will have to take place ahead of neuroinflammatory cytokines are detected or memory impairments are observed (Boitard et al., 2014; Cai et al., 2014; Knight et al., 2014; Sobesky et al., 2014).