The molecular pathogenesis underlying anxiety disorders is still unclear. Here, the authors demonstrate that myristoylated alanine-rich C-kinase substrate like 1 (MARCKSL1) overexpression in mice increases spine formation in the amygdala and induces stress hormone upregulation and anxiety-like behaviors. Suppression of MARCKSL1 in the amygdala ameliorates both the increase in stress hormones and the elevated anxiety-like behaviors. Our results indicate that MARCKSL1 expression in the amygdala plays an important role in anxiety-like behaviors.
This was proved, in part, by the knockdown of MARCKSL1 in vivo in mice using our i-FectTM. Tanaka, Takashi; Shimizu, Shoko; Ueno, Masaki; Fujihara, Yoshitaka; Ikawa, Masahito; Miyata, Shingo. MARCKSL1 Regulates Spine Formation in the Amygdala and Controls the Hypothalamic-Pituitary-Adrenal Axis and Anxiety-Like Behaviors. https://doi.org/10.1016/j.ebiom.2018.03.018
Figure: Knockdown of MARCKSL1 ameliorates anxiety-like behavior in MARCKSL1 Tg mice. (A and B) For the in vivo experiment, siRNA (blue) was injected into the CeA (total 4 sites) with i-Fect siRNA transfection reagents 5 days prior to behavioral tests. (C) In situ hybridization for Marcksl1 mRNA (blue) in the amygdala after injection of Marcksl1 siRNA into the CeA of Tg/Tg mice. Scale bar, 200 μm. (D and E) Light/dark transition test and elevated plus maze performance in
MARCKSL1 knockdown mice (WT + control siRNA, n = 7; Tg/Tg + control siRNA, n = 7; Tg/Tg + Marcksl1 siRNA, n = 8).
We will continue to post new i-Fect results here.
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