作者: Maximilian Lenz , Amelie Eichler , Pia Kruse , Andreas Strehl , Silvia Rodriguez-Rozada
DOI: 10.1101/2020.10.16.336065
关键词: Neurotransmission 、 Synaptic plasticity 、 Stimulation 、 Long-term potentiation 、 Neuroscience 、 Tumor necrosis factor alpha 、 Hippocampal formation 、 Excitatory postsynaptic potential 、 Chemistry 、 Brain stimulation
摘要: ABSTRACT Systemic inflammation is associated with alterations in complex brain functions such as learning and memory. However, diagnostic approaches to functionally assess quantify inflammation-associated synaptic plasticity are not well-established. In previous work, we demonstrated that bacterial lipopolysaccharide (LPS)-induced systemic alters the ability of hippocampal neurons express plasticity, i.e., long-term potentiation (LTP) excitatory neurotransmission. Here, tested whether induced by repetitive magnetic stimulation (rMS), a non-invasive technique used clinical practice, affected LPS-induced inflammation. Specifically, explored tissue cultures learn more about direct effects LPS on neural tissue, for plasticity-restoring anti-inflammatory cytokine interleukin 10 (IL10). As shown previously, Hz (rMS) organotypic entorhino-hippocampal robust increase neurotransmission onto CA1 pyramidal neurons. Furthermore, LPS-treated did rMS-induced plasticity. Live-cell microscopy prepared from novel transgenic reporter mouse line [C57BL6-Tg(TNFa-eGFP)] confirms ex vivo administration triggers microglial tumor necrosis factor alpha (TNFα) expression, which ameliorated presence IL10. Consistent this observation, IL10 hampers TNFα, IL6, IL1β, IFNγ restores LPS. These findings establish suitable model studying inflammation-induced thus providing biological basis use transcranial context