Fig. 2: Effects of prenatal ethanol exposure (PEE, 4 g/kg per day) on hippocampal morphology, glutamatergic and GABAergic neuron numbers, and mRNA expression of insulin-like growth factor 1 (IGF1) signalling pathway-related genes and N-methyl-D-aspartate-subtype glutamate receptors (NRs) without and after chronic stress in male adult offspring rats. | Cell Death & Disease

Fig. 2: Effects of prenatal ethanol exposure (PEE, 4 g/kg per day) on hippocampal morphology, glutamatergic and GABAergic neuron numbers, and mRNA expression of insulin-like growth factor 1 (IGF1) signalling pathway-related genes and N-methyl-D-aspartate-subtype glutamate receptors (NRs) without and after chronic stress in male adult offspring rats.

From: Programming for increased expression of hippocampal GAD67 mediated the hypersensitivity of the hypothalamic–pituitary–adrenal axis in male offspring rats with prenatal ethanol exposure

Fig. 2

a Morphologic changes in the whole hippocampus (HE, × 100), granular cells in the dentate gyrus (DG) areas and pyramidal cells in the cornu ammonis 3 (CA3) (HE, × 200). There were only a few neuronal nuclei in the CA3 region that were dense and darkly stained in the PEE group both without and after CS. b–e Hippocampal IGF1, IGF1 receptor (IGF1R), protein kinase B (AKT1) and synapsin 1 mRNA expression. f Photomicrographs of immunofluorescence-labelled glutamatergic neurons (glutamate, red), GABAergic neurons (GAD67, red) and neurons (NeuN, green). Scale bars = 200 μm. g–j Quantitative analysis of the glutamatergic or GABAergic neurons in the hippocampal CA3 and DG areas; three brain sections from the same levels of the hippocampus were selected from each animal and quantified. k, l Hippocampal glutamate and gamma aminobutyric acid (GABA) concentrations. m–o Hippocampal NR1, NR2A, and NR2B expression. Mean ± S.E.M., n = 8 offspring from eight litters. *P < 0.05, **P < 0.01 vs. control; #P < 0.05, ##P < 0.01 vs. without stress

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