Although in vitro endoplasmic reticulum (ER) stress studies have been carried out using Tunicamycin in human trophoblast cell lines in recent years, the effect of calcium homeostasis impaired by the effect of Thapsigargin on cell survival - death pathways have not been clearly demonstrated. Here, the effects of ER stress and impaired calcium homeostasis on cell death pathways such as apoptosis and autophagy in 2-dimensional and 3-dimensional cell cultures were investigated using the HTR8 / SVneo cell line representing human trophoectoderm cells and the ER stressor Thapsigargin. By using Real Time PCR, gene and immunofluorescence analyzes were studied at the protein level. In this study, it has been established that the Thapsigargin creates ER stress by increasing the level of GRP78 gene and protein in 2 and 3 dimensions of human trophoectoderm cells and that cells show different characterization properties in 2 and 3 dimensions. It has been determined that while it moves in the direction of EIF2A and IRE1A mechanisms in 2 dimensions, it proceeds in the direction of EIF2A and ATF6 mechanisms in 3 dimensions and creates different responses in survival and programmed cell death mechanisms such as apoptosis and autophagy. With forthcoming studies, it is thought that the effects of Thapsigargin on the intrinsic pathway of apoptosis and the linkage of the autophagy mechanism, the examination of the survival-death pathways in the co-culture model with endometrial cells, therapeutic target molecules that will contribute to the elucidation of intracellular cell dynamics may increase the success of implantation.

Objectives: This study aimed to investigate the effects of prenatal stress (PS) on hippocampus of early acute pentylenetetrazole (PTZ)-kindled offspring in adolescence. Recognition memory, morphological changes and synaptophysin levels in hippocampus were evaluated. Methods: Restraint stress was induced to a group of pregnant dams and non-stressed (NA) group remained undisturbed. Next, male and female offspring were divided as 1. PS-PTZ, 2. PS -control, 3. NA-PTZ and 4. NA-control (n = 12 in each group). The object recognition test was performed following PTZ injection (45 mg/kg) on postnatal day 10 (P10). Brains were collected on postnatal day 35 (P35) to determine neuronal density and synaptophysin expression by immuno/-histological studies. Further, oxidative stress products in hippocampus were analyzed with different biochemical assays. Results: PS impaired recognition memory in PTZ group significantly (p = 0.03); however, the impairment of PS was reversible in control group compared to PTZ (p = 0.04). Furthermore, PS caused neuronal loss in CA1 (p = 0.01) and decreased synaptophysin expression in the CA3 area of hippocampus in PTZ group (p = 0.03). PS also increased the oxidative stress markers in PTZ group significantly (p < 0.05). Conclusions: These results suggest that PS causes neurodevelopmental deficits in adolescent hippocampus and recognition memory after early-life seizures prominently. However, the damage of only PS in adolescence can be reversible. Therefore, the effects of PS in the adult hippocampus and other regions of brain need to be further studied

Objectives The present study aimed to investigate the effects of acute hypoxia exposure following prenatal stress on the novelty‐seeking behavior and hippocampus of adolescent rats. Methods The offspring were divided into prenatal stress (PS) and non‐stress (NS) groups. Both groups were exposed to hypoxia on postnatal day 10 (P10) while control groups were undisturbed. Novel object recognition task was performed in each group. Next, brains were collected to examine hippocampus via immunohistochemical and biochemical studies on postnatal day 35 (P35). Results PS decreased novelty discrimination and synaptophysin (SYN) expressions in both CA1 and CA3 of the hypoxia group prominently (p < 0.05). Nestin‐expressing cells were reduced while vascular endothelial growth factor (VEGF) expression was enhanced in the subgranular zone (SGZ) of PS‐hypoxia group (p < 0.05). VEGF enhancement triggered angiogenesis in the CA1 and CA3 significantly (p < 0.05). PS also increased thiobarbituric acid reactive substances (TBARS) levels in the hypoxia group as a result of oxidative stress (p < 0.05). Conclusion These findings demonstrated that PS exacerbates neurodevelopmental deficits in the hippocampus of acute hypoxia‐induced offspring in adolescence.

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