Browsing by Subject "MORRIS WATER MAZE"

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  • Komulainen, Emilia; Varidaki, Artemis; Kulesskaya, Natalia; Mohammad, Hasan; Sourander, Christel; Rauvala, Heikki; Coffey, Eleanor T. (2020)
    The protein kinase JNK1 exhibits high activity in the developing brain, where it regulates dendrite morphology through the phosphorylation of cytoskeletal regulatory proteins. JNK1 also phosphorylates dendritic spine proteins, and Jnk1-/- mice display a long-term depression deficit. Whether JNK1 or other JNKs regulate spine morphology is thus of interest. Here, we characterize dendritic spine morphology in hippocampus of mice lacking Jnk1-/- using Lucifer yellow labelling. We find that mushroom spines decrease and thin spines increase in apical dendrites of CA3 pyramidal neurons with no spine changes in basal dendrites or in CA1. Consistent with this spine deficit, Jnk1-/- mice display impaired acquisition learning in the Morris water maze. In hippocampal cultures, we show that cytosolic but not nuclear JNK, regulates spine morphology and expression of phosphomimicry variants of JNK substrates doublecortin (DCX) or myristoylated alanine-rich C kinase substrate-like protein-1 (MARCKSL1), rescue mushroom, thin, and stubby spines differentially. These data suggest that physiologically active JNK controls the equilibrium between mushroom, thin, and stubby spines via phosphorylation of distinct substrates.
  • Stanelle-Bertram, Stephanie; Walendy-Gnirss, Kerstin; Speiseder, Thomas; Thiele, Swantje; Asante, Ivy Asantewaa; Dreier, Carola; Kouassi, Nancy Mounogou; Preuss, Annette; Pilnitz-Stolze, Gundula; Mueller, Ursula; Thanisch, Stefanie; Richter, Melanie; Scharrenberg, Robin; Kraus, Vanessa; Doerk, Ronja; Schau, Lynn; Herder, Vanessa; Gerhauser, Ingo; Pfankuche, Vanessa Maria; Kaeufer, Christopher; Waltl, Inken; Moraes, Thais; Sellau, Julie; Hoenow, Stefan; Schmidt-Chanasit, Jonas; Jansen, Stephanie; Schattling, Benjamin; Ittrich, Harald; Bartsch, Udo; Renne, Thomas; Bartenschlager, Ralf; Arck, Petra; Cadar, Daniel; Friese, Manuel A.; Vapalahti, Olli; Lotter, Hanna; Benites, Sany; Rolling, Lane; Gabriel, Martin; Baumgaertner, Wolfgang; Morellini, Fabio; Hoelter, Sabine M.; Amarie, Oana; Fuchs, Helmut; de Angelis, Martin Hrabe; Loescher, Wolfgang; de Anda, Froylan Calderon; Gabriel, Guelsah (2018)
    Congenital Zika virus (ZIKV) syndrome may cause fetal microcephaly in -1% of affected newborns. Here, we investigate whether the majority of clinically inapparent newborns might suffer from long-term health impairments not readily visible at birth. Infection of immunocompetent pregnant mice with high-dose ZIKV caused severe offspring phenotypes, such as fetal death, as expected. By contrast, low-dose (LD) maternal ZIKV infection resulted in reduced fetal birth weight but no other obvious phenotypes. Male offspring born to LD ZIKV-infected mothers had increased testosterone (TST) levels and were less likely to survive in utero infection compared to their female littermates. Males also presented an increased number of immature neurons in apical and basal hippocampal dendrites, while female offspring had immature neurons in basal dendrites only. Moreover, male offspring with high but not very high (storm) TST levels were more likely to suffer from learning and memory impairments compared to females. Future studies are required to understand the impact of TST on neuropathological and neurocognitive impairments in later life. In summary, increased sex-specific vigilance is required in countries with high ZIKV prevalence, where impaired neurodevelopment may be camouflaged by a healthy appearance at birth.
  • Leppä, Elli; Linden, Anni-Maija; Vekovischeva, Olga Y.; Swinny, Jerome D.; Rantanen, Ville; Toppila, Esko; Hoeger, Harald; Sieghart, Werner; Wulff, Peer; Wisden, William; Korpi, Esa R. (2011)