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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

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

Fig. 1

GABA and Ki67 immunohistochemistry in the brains of FASD and controls at early developmental stages and at mid-gestation. Similar GABA interneuron density in cortical plate of FASD and controls at 14-16 WG which contains bipolar INs migrating along the perforating microvessels as indicated by arrows (a, b) [OM × 200], contrasting with the low number of GABA interneurons in the VZ/SVZ (c, d) [OM x200], and in the GE in FASD compared to control brains (e, f) [OM x100)]. At 20 WG, GABA interneurons were scarce in the cortical plate of FASD compared to control (g, h) [OM x 200], in the VZ/SVZ (i, j) [OM x 200] and in the GE (k, l) [OM x 200]. Low proliferative activity revealed by Ki67 immunohistochemistry in the GE of the FASD brains aged 20 and 22 WG compared to control brains (m-r) [OM x 100]. CP: cortical plate; CTRL: control cases; GE: ganglionic eminence; FASD: foetal alcohol spectrum disorder; OM: original magnification; SVZ: cortical subventricular zone

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