Figure 3
From: Establishment of Novel Murine Model showing Vascular Inflammation-derived Cognitive Dysfunction
Vascular inflammation induced by abdominal aortic aneurysm accelerates synaptic and cognitive dysfunction in middle-aged mice. (A–D) Morris water maze test in 3-month- (young, Y) and 12-month- (middle-aged, M) old mice at 4 weeks after sham operation (Sham) or angiotensin II (AngII) infusion with calcium chloride (CaCl2) application (CaCl2 + AngII). (A) M mice after CaCl2 + AngII showed significant impairment of escape latency in the hidden platform trial. (B,C) Swim time spent (B) and number of platform crossings (C) in target quadrant (TQ) vs. other quadrants (OQs). Values of the three OQs were combined and averaged. (D) Representative searching strategy in the probe test. (E) Slope of fEPSP decreased in M mice after CaCl2 + AngII. (F) Representative low- and high-power photomicrographs of sections of hippocampal CA3 and CA1 regions with Nissl and NeuN staining. (G,H) Quantification of hippocampal neuronal populations in CA3(G) and CA1(H) regions. *p < 0.05, **p < 0.01, ***p < 0.001. Scale bar = 100 µm. n = 7 for Y [Sham], n = 10 for Y [CaCl2 + AngII], n = 7 for M [Sham] and n = 7 for M [CaCl2 + AngII] (A–D); n = 16 for Y [Sham], n = 14 for Y [CaCl2 + AngII], n = 9 for M [Sham] and n = 10 for M [CaCl2 + AngII] (E); n = 5 mice/group (F–H).
