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. 2019 Jul 30;10:955. doi: 10.3389/fphys.2019.00955

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Copyright © 2019 Stolp, Fleiss, Arai, Supramaniam, Vontell, Birtles, Yates, Baburamani, Thornton, Rutherford, Edwards and Gressens.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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P5 mice with inflammation-induced brain damage also show altered interneuron development across the cortex. Cortical development was assessed based on immunohistochemistry for general microstructure (DAPI), developing cortical neurons (CTIP2) and interneuron subpopulations at P5 (A,B). A significant decrease in Reelin and Calretinin (CalR)-positive neurons was observed in the whole cortex (C), but no change in CTIP2 positive pyramidal neurons (B). Assessment of the less prevalent interneuron populations according to upper (II–IV) or lower (V, VI) cortical layer distribution showed a small but significant increase the majority of interneuron populations in the lower layers (treatment effect, p = 0.04, two-way ANOVA) and no significant change in the upper layers (D,E). Data presented as mean ± SD; scale bar = 100 μm. ^*p < 0.05, ^***p < 0.001. CalR, calretinin; PV, parvalbumin; SST, somatostatin; NPY, Neuropeptide Y; CalB, calbindin.