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@ARTICLE{Schott:155635,
      author       = {Schott, Björn and Kronenberg, Golo and Schmidt, Ulrike and
                      Düsedau, Henning P and Ehrentraut, Stefanie and Geisel,
                      Olga and von Bohlen Und Halbach, Oliver and Gass, Peter and
                      Dunay, Ildiko Rita and Hellweg, Rainer},
      title        = {{R}obustly {H}igh {H}ippocampal {BDNF} levels under {A}cute
                      {S}tress in {M}ice {L}acking the {F}ull-length p75
                      {N}eurotrophin {R}eceptor.},
      journal      = {Pharmacopsychiatry},
      volume       = {54},
      number       = {5},
      issn         = {1439-0795},
      address      = {Stuttgart [u.a.]},
      publisher    = {Thieme},
      reportid     = {DZNE-2021-00803},
      pages        = {205-213},
      year         = {2021},
      abstract     = {Brain-derived neurotrophic factor (BDNF) exerts its effects
                      on neural plasticity via 2 distinct receptor types, the
                      tyrosine kinase TrkB and the p75 neurotrophin receptor
                      (p75NTR). The latter can promote inflammation and cell death
                      while TrkB is critically involved in plasticity and memory,
                      particularly in the hippocampus. Acute and chronic stress
                      have been associated with suppression of hippocampal BDNF
                      expression and impaired hippocampal plasticity. We
                      hypothesized that p75NTR might be involved in the
                      hippocampal stress response, in particular in stress-induced
                      BDNF suppression, which might be accompanied by increased
                      neuroinflammation.We assessed hippocampal BDNF protein
                      concentrations in wild-type mice compared that in mice
                      lacking the long form of the p75NTR (p75NTRExIII-/-) with or
                      without prior exposure to a 1-hour restraint stress
                      challenge. Hippocampal BDNF concentrations were measured
                      using an optimized ELISA. Furthermore, whole-brain mRNA
                      expression of pro-inflammatory interleukin-6 (Il6) was
                      assessed with RT-PCR.Deletion of full-length p75NTR was
                      associated with higher hippocampal BDNF protein
                      concentration in the stress condition, suggesting
                      persistently high hippocampal BDNF levels in
                      p75NTR-deficient mice, even under stress. Stress elicited
                      increased whole-brain Il6 mRNA expression irrespective of
                      genotype; however, p75NTRExIII-/- mice showed elevated
                      baseline Il6 expression and thus a lower relative
                      increase.Our results provide evidence for a role of p75NTR
                      signaling in the regulation of hippocampal BDNF levels,
                      particularly under stress. Furthermore, p75NTR signaling
                      modulates baseline but not stress-related Il6 gene
                      expression in mice. Our findings implicate p75NTR signaling
                      as a potential pathomechanism in BDNF-dependent modulation
                      of risk for neuropsychiatric disorders.},
      keywords     = {Animals / Brain-Derived Neurotrophic Factor: genetics /
                      Brain-Derived Neurotrophic Factor: metabolism / Hippocampus:
                      metabolism / Mice / Receptor, Nerve Growth Factor:
                      metabolism / Receptors, Nerve Growth Factor: genetics /
                      Receptors, Nerve Growth Factor: metabolism / Signal
                      Transduction},
      cin          = {AG Fischer 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33592642},
      doi          = {10.1055/a-1363-1680},
      url          = {https://pub.dzne.de/record/155635},
}