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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: Prenatal alcohol exposure is a leading cause of interneuronopathy in humans

Fig. 2

Schematic representation of GABA and CR containing interneurons in the GE, VZ/SVZ and in the cortical plate of FASD and control brains during foetal and post-natal life. (a) Evolution of GABA interneuron density in the GE and VZ/SVZ obtained from semi-quantitative immunohistochemical evaluation. The vertical dotted line indicates the stage from which no significant differences between FASD and controls were observed (26 WG). Between 20 and 26 WG, an intense generation of GABA-positive cells was observed in control brains. (b) Evolution of CR interneuron density in the GE and VZ/SVZ obtained from semi-quantitative immunohistochemical evaluation. The vertical dotted line indicates the stage at which no significant differences between FASD and controls were observed (24 WG). Between 20 and 24 WG, an intense generation of CR-positive cells was observed in control brains and after 24 WG, two smaller peaks of production were observed in FASD brains indicating a production delay of two months. (c) Evolution of cortical density in GABA interneurons. Before 26 WG, cortical interneuron density was lower in FASD, from 26 WG to birth, no major differences were observed between FASD and controls. After birth, cortical density was slightly increased in FASD. (d) Evolution of cortical density in CR interneurons. Before birth, the density of CR interneurons was constantly lower in FASD cortices with a reverse pattern after birth, indicating a delayed settling of CR interneurons in the cortex of FASD

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