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. Author manuscript; available in PMC: 2021 Apr 19.
Published in final edited form as: Neuron. 2007 Sep 6;55(5):697–711. doi: 10.1016/j.neuron.2007.07.025

Figure 1. Remodeling of inhibitory circuits and alterations in the expression of NPY and its receptors in the dentate gyrus of hAPP-J20 mice.

Figure 1.

(A) Brain sections were immunoperoxidase-stained for NPY. Compared with NTG controls, hAPP-J20 mice had an increase in NPY expression in the molecular layer of the dentate gyrus (arrow) and in the mossy fibers (arrowhead). (B) Confocal microscopic imaging of sections double-labeled for calbindin (red) and NPY (green) demonstrated sprouting of NPY axons in the molecular layer (arrow), ectopic expression of NPY in mossy fibers (arrowheads), and severe depletion of calbindin (CB) in granule cells of an hAPP-J20 mouse. Images represent the regions indicated by squares in panel A. (C–D) Calbindin depletions correlated with NPY increases in the dentate gyrus (C) and mossy fibers (D) in hAPP-J20 mice. (E) In situ hybridization revealed ectopic expression of NPY mRNA in granule cells (arrow) of an hAPP-J20 mouse (bottom panel). (F) Compared with NTG mice, hAPP-J20 mice had sprouting of somatostatin (SOM)-positive axons in the molecular layer (top panels), which was quantitated by densitometry (bottom panel). (G) Axonal sprouts in the molecular layer of hAPP-J20 mice were double-labeled for NPY (green) and SOM (red), indicating that they originated from hilar GABAergic cells. (H) NPY receptors in the dentate gyrus were also altered in hAPP-J20 mice, as determined by quantitative fluorogenic RT-PCR: Y1 receptors were decreased, whereas Y2 receptors were increased compared with NTG controls. Numbers in bars indicate number of mice per group. *P<0.05, **P<0.01, ***P<0.001 vs. NTG by Student’s t test.