TY  - JOUR
A1  - Lenz, Maximilian
A1  - Eichler, Amelie
A1  - Kruse, Pia
A1  - Strehl, Andreas
A1  - Rodriguez-Rozada, Silvia
A1  - Goren, Itamar
A1  - Yogev, Nir
A1  - Frank, Stefan
A1  - Waisman, Ari
A1  - Deller, Thomas
A1  - Jung, Steffen
A1  - Maggio, Nicola
A1  - Vlachos, Andreas
T1  - Interleukin 10 restores lipopolysaccharide-induced alterations in synaptic plasticity probed by repetitive magnetic stimulation
T2  - Frontiers in immunology
N2  - Systemic inflammation is associated with alterations in complex brain functions such as learning and memory. However, diagnostic approaches to functionally assess and quantify inflammation-associated alterations in synaptic plasticity are not well-established. In previous work, we demonstrated that bacterial lipopolysaccharide (LPS)-induced systemic inflammation alters the ability of hippocampal neurons to express synaptic plasticity, i.e., the long-term potentiation (LTP) of excitatory neurotransmission. Here, we tested whether synaptic plasticity induced by repetitive magnetic stimulation (rMS), a non-invasive brain stimulation technique used in clinical practice, is affected by LPS-induced inflammation. Specifically, we explored brain tissue cultures to learn more about the direct effects of LPS on neural tissue, and we tested for the plasticity-restoring effects of the anti-inflammatory cytokine interleukin 10 (IL10). As shown previously, 10 Hz repetitive magnetic stimulation (rMS) of organotypic entorhino-hippocampal tissue cultures induced a robust increase in excitatory neurotransmission onto CA1 pyramidal neurons. Furthermore, LPS-treated tissue cultures did not express rMS-induced synaptic plasticity. Live-cell microscopy in tissue cultures prepared from a novel transgenic reporter mouse line [C57BL/6-Tg(TNFa-eGFP)] confirms that ex vivo LPS administration triggers microglial tumor necrosis factor alpha (TNFα) expression, which is ameliorated in the presence of IL10. Consistent with this observation, IL10 hampers the LPS-induced increase in TNFα, IL6, IL1β, and IFNγ and restores the ability of neurons to express rMS-induced synaptic plasticity in the presence of LPS. These findings establish organotypic tissue cultures as a suitable model for studying inflammation-induced alterations in synaptic plasticity, thus providing a biological basis for the diagnostic use of transcranial magnetic stimulation in the context of brain inflammation.
Y1  - 2020
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/57556
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-575561
SN  - 1664-3224
VL  - 11
IS  - Article 614509
PB  - Frontiers Media
CY  - Lausanne
ER  -