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Figure 4 | Molecular Neurodegeneration

Figure 4

From: Nitrosamine exposure exacerbates high fat diet-mediated type 2 diabetes mellitus, non-alcoholic steatohepatitis, and neurodegeneration with cognitive impairment

Figure 4

Hippocampus and Temporal Lobe Degeneration Following NDEA-Exposure and/or HFD Feeding: Long Evans rats treated with NDEA or vehicle (Veh) by i.p. injection (N = 12/group), and then chronically fed with high fat (HFD) or low fat (LFD) containing chow for 6 weeks (see Figure Legend 1). Brains were immersion fixed and embedded in paraffin. Histological sections were stained with Luxol fast blue, H&E. Blue staining corresponds to myelinated fibers and tracts. Photomicrographs depict (A-D) low magnification images of temporal cortex (TC) and hippocampal formation and (E-H) high magnification images of the temporal cortex. Note the thinning/reduced cell density within the CA1 region (Segment 1 of Ammon's Horn; arrows) of the hippocampal formation and slight thinning of the TC in brains of (B) Veh+HFD, (C) NDEA+LFD, and (D) NDEA+HFD treated rats relative to control (A) Veh+LFD). Higher magnification images of TC show (E) abundant pyramidal neurons (N) with regular organization and scattered glia (gl) in LFD+Veh treated control brains, (F) neuronal atrophy and apoptosis (N; arrows) and increased glia (gl) in Veh+HFD treated rats, and (G, H) conspicuous neuronal loss with small clusters of apoptotic cells (encircled) in NDEA ± HFD-treated rats. In addition, as observed in the HFD-fed rat brains, glial cells were conspicuously increased relative to neurons in the (H) HFD+NDEA treated temporal cortex. Original magnifications: A-D, 40×; E-H, 400×. (Scale bar A-D, 200 microns; E-H 25 microns).

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