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The Transgenerational Effects of Prenatal Synthetic Glucocorticoids on the Hippocampus Cortex

ABSTRACT: The Transgenerational Effects of Prenatal Synthetic Glucocorticoids on the Hippocampus Cortex

PROVIDER: PRJNA431992 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6519270.fastq.gz	Fastqsanger.gz
	SRR6519280.fastq.gz	Fastqsanger.gz
	SRR6519290.fastq.gz	Fastqsanger.gz
	SRR6519300.fastq.gz	Fastqsanger.gz
	SRR6519310_1.fastq.gz	Fastqsanger.gz

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Project description:First generation animals (F1) were exposed to multiple courses of synthetic glucocorticoids in utero. Animals were then bred to produce second (F2) and third (F3) generation offspring. These animals underwent behavioural assessmenets before sacrifice. In this experiment the prefrontal cortex for F1, F2, and F3 female animals, as well as F1 males (Control and sGC) have been extracted via micro-punch and RNA has been extracted.

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Project description:Approximately 10% of pregnant women are at risk of preterm delivery and receive synthetic glucocorticoids (sGC) to promote fetal lung development. Studies have indicated that prenatal sGC therapy modifies hypothalamic-pituitary-adrenal (HPA) function in first-generation (F(1)) offspring. The objective of this study was to determine whether differences in HPA function and behavior are evident in the subsequent (F(2)) generation. Pregnant guinea pigs (F(0)) received betamethasone (BETA; 1 mg/kg) or saline on gestational d 40/41, 50/51, and 60/61. F(1) females were mated with control males to create F(2) offspring. HPA function was assessed in juvenile and adult F(2) offspring. Locomotor activity was assessed in juvenile offspring. Analysis of HPA-related gene expression was undertaken in adult hippocampi, hypothalami, and pituitaries. Locomotor activity was reduced in F(2) BETA males (P < 0.05). F(2) BETA offspring displayed blunted cortisol response to swim stress (P < 0.05). After dexamethasone challenge, F(2) BETA males and females displayed increased and decreased negative feedback, respectively. F(2) BETA females had reduced pituitary levels of proopiomelanocortin (and adrenocorticotropic hormone), and corticotropin-releasing hormone receptor mRNA and protein (P < 0.05). F(2) BETA males displayed increased hippocampal glucocorticoid receptor (P < 0.001), whereas in BETA females, hippocampal glucocorticoid receptor and mineralocorticoid receptor mRNA were decreased (P < 0.05). In conclusion, prenatal BETA treatment affects HPA function and behavior in F(2) offspring. In F(2) BETA females, pituitary function appears to be primarily affected, whereas hippocampal glucocorticoid feedback systems appear altered in both F(2) BETA males and females. These data have clinical implication given the widespread use of repeat course glucocorticoid therapy in the management of preterm labour.

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