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Fig. 6 | Translational Neurodegeneration

Fig. 6

From: Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer’s disease

Fig. 6

Dense parvalbumin dendritic connective zone in TgF344-AD rats in contrast with atrophic somatostatin interneurons. We further probed the hippocampal GABAergic network in TgF344-AD rats through neuronal tracing with Sholl analyses to determine the dendritic complexity (branching intersections by distance from soma). SST and PVB neurons were assessed in CA1 and DG in NTgs and Tgs at 9, 12 and 15 months of age. No significant differences were detected in CA1 SST dendritic complexity at 9 (a, b) and 12 months (c), but there was a loss of complexity in 15-month-old Tgs (d). eh In the DG, Tg SST interneurons had decreased intersections at all ages, indicative of vast neuronal atrophy. il For CA1 PVB interneurons, increased dendritic complexity was detected in Tgs at 9 months (i and j) and 12 months (significant genotype × distance interaction: P = 0.03; k), but the dendritic complexity was decreased compared to NTgs at 15 months (l). Notably, the DG PVB neurons of Tg rats exhibited a large increase in dendritic complexity near cell somas at 9 (m and n) and 12 months (o), and a robust loss of complexity at 15 months (p), compared to NTgs. a, e, i, and m Representative neuronal traces at 9 months demonstrate no change in CA1 SST, decreased DG SST dendritic length and complexity in Tgs, and increased PVB dendritic length and complexity in the Tg CA1 and DG. Red arrows indicate cell soma. Scale bar, 50 μm. Abbreviations: corpus callosum (cc); dorsal/ventral molecular layer (d/v mol); granular cell layer (GCL); pyramidal layer (PL). Data are mean ± SEM (from n = 16 cells/cohort, sampled across 4 rats/genotype at each age); repeated measures ANOVA with Holm-Sidak post hoc test; *P < 0.05, **P < 0.01, ***P < 0.001

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