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. 2018 Aug 16;13(8):e0202566. doi: 10.1371/journal.pone.0202566

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© 2018 Bilkei-Gorzo et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 6 — (A) Representative photomicrographs of GFAP- and TNFα-immunopositive astrocytes in the stratum lacunosum moleculare layer of the CA1 hippocampal region of 24-months-old GABA-Cnr1^+/+ and GABA-Cnr1^−/− mice, respectively. Scale bars, 25 μm. Negative controls were stained without the anti-TNFα antibody. (B) Age-related increase in astrocytic TNFα levels is exacerbated in GABA-Cnr1^−/− mice. n = 42–60 per age and genotype. +++ p < 0.001 significantly different compared to GABA-Cnr1^+/+ mice from the same age group. ** p < 0.01; *** p < 0.001 significantly differs from 2-months-old mice with the same genotype. Columns represent mean values, error bars standard error of means (SEM). (C) Positive relation between the number of GFAP-positive processes and TNFα-immunoreactivity in hippocampal astrocytes of 24 months-old GABA-Cnr1^-/- and GABA-Cnr1^+/+ mice; n = 105.