کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6017747 | 1580171 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Systemic inflammation is associated with a reduction in Synaptopodin expression in the mouse hippocampus
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
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چکیده انگلیسی
Systemic inflammation is known to affect memory function through the activation of immune cells and the release of inflammatory cytokines. However, the neuronal targets by which inflammatory signaling pathways affect synaptic plasticity remain not well understood. Here, we addressed the question of whether systemic lipopolysaccharide (LPS)-induced inflammation influences the expression of Synaptopodin (SP). SP is an actin-binding protein, which is considered to control the ability of neurons to express synaptic plasticity by regulating the actin-cytoskeleton and/or intracellular Ca2Â + stores. This makes SP an interesting target molecule in the context of inflammation-induced alterations in synaptic plasticity. Using quantitative PCR (qPCR)-analysis and immunohistochemistry we here demonstrate that intraperitoneal LPS-injection in two-month old male Balb/c mice leads to a reduction in hippocampal SP-levels (area CA1; 24Â h after injection). These changes are accompanied by a defect in the ability to induce long-term potentiation (LTP) of Schaffer collateral-CA1 synapses, similar to what is observed in SP-deficient mice. We therefore propose that systemic inflammation could exert its effects on neural plasticity, at least in part, through the down-regulation of SP in vivo.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 261, November 2014, Pages 230-235
Journal: Experimental Neurology - Volume 261, November 2014, Pages 230-235
نویسندگان
Andreas Strehl, Maximilian Lenz, Zeev Itsekson-Hayosh, Denise Becker, Joab Chapman, Thomas Deller, Nicola Maggio, Andreas Vlachos,