Genetic and neuroendocrine regulation of the postpartum brain

Gammie, Stephen C.; Driessen, Terri M.; Zhao, Changjiu; Saul, Michael C.; Eisinger, Brian E.

doi:10.1016/j.yfrne.2016.05.002

Cited by 32 publications

(42 citation statements)

References 162 publications

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“…The brain is an organ that serves as the central nervous system among all vertebrate. Stroke is caused by occulusion of cerebral vessels or angiorhagia 1 - 4 . It is reported that stroke is the primary cause of disability and affects approximately 795,000 people annually.…”

Section: Introductionmentioning

confidence: 99%

AMPK: Potential Therapeutic Target for Ischemic Stroke

et al. 2018

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5'-AMP-activated protein kinase (AMPK), a member of the serine/threonine (Ser/Thr) kinase group, is universally distributed in various cells and organs. It is a significant endogenous defensive molecule that responds to harmful stimuli, such as cerebral ischemia, cerebral hemorrhage, and, neurodegenerative diseases (NDD). Cerebral ischemia, which results from insufficient blood flow or the blockage of blood vessels, is a major cause of ischemic stroke. Ischemic stroke has received increased attention due to its '3H' effects, namely high mortality, high morbidity, and high disability. Numerous studies have revealed that activation of AMPK plays a protective role in the brain, whereas its action in ischemic stroke remains elusive and poorly understood. Based on existing evidence, we introduce the basic structure, upstream regulators, and biological roles of AMPK. Second, we analyze the relationship between AMPK and the neurovascular unit (NVU). Third, the actions of AMPK in different phases of ischemia and current therapeutic methods are discussed. Finally, we evaluate existing controversy and provide a detailed analysis, followed by ethical issues, potential directions, and further prospects of AMPK. The information complied here may aid in clinical and basic research of AMPK, which may be a potent drug candidate for ischemic stroke treatment in the future.

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Section: Introductionmentioning

confidence: 99%

AMPK: Potential Therapeutic Target for Ischemic Stroke

et al. 2018

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“…In order to become maternal, the expression of hundreds of genes changes in the peripartum period . These changes are the bases for the numerous physiological, cellular and molecular adaptations the female has to go through in order to be prepared for the upcoming challenges as a mother.…”

Section: Introductionmentioning

confidence: 99%

“…4 In order to become maternal, the expression of hundreds of genes changes in the peripartum period. 5 These changes are the bases for the numerous physiological, cellular and molecular adaptations the female has to go through in order to be prepared for the upcoming challenges as a mother. Among these changes are increased signaling of the brain neuropeptide systems of oxytocin and vasopressin; while oxytocin has been known as a maternal neuropeptide since the 1980s, 6,7 vasopressin has been finally proven as such only in the last decade.…”

Section: Introductionmentioning

confidence: 99%

Brain vasopressin signaling modulates aspects of maternal behavior in lactating rats

Bayerl

Bosch

2018

Genes Brain and Behavior

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The brain vasopressin system mediates various social behaviors as has been studied mostly in males. Only recently, advances in social neuroscience revealed that central vasopressin signaling via its V1a and V1b receptors also facilitates female social behavior, including maternal behavior. In this review, we show how maternal care, maternal motivation and maternal aggression of lactating rat mothers are modulated in a V1 receptor subtype- and brain region-specific manner. Measuring local release pattern of vasopressin via intracerebral microdialysis in the behaving rat mother as well as using pharmacological approaches to activate or block vasopressin receptors with subsequent behavioral observation provide detailed insight into the functional role of the vasopressin system in maternal behavior. In this context, the complementary rat animal model of high (HAB) and low anxiety-related behavior (LAB) is particularly helpful due to the genetically determined high activity of the vasopressin gene in HAB rats, which also underlies their high levels of maternal behavior. Furthermore, first studies in humans indicate that the vasopressin system in general and the V1a receptor in more particular might mediate mothering.

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“…qPCR analysis was performed for five of the most highly-differentially expressed genes from [Moura et al, 2016;Gammie et al, 2016]. Whilst the direction of expression difference was generally consistent across the microarray and qPCR analyses for these genes, only two genes (Cyp2g1 and Stoml3)…”

Section: Quantitative Pcr (Qpcr)mentioning

confidence: 95%

Brain gene expression in a novel mouse model of postpartum mood disorder

Humby

Davies

2019

Preprint

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Introduction: Steroid sulfatase (STS) is an enzyme which cleaves sulfate groups from a variety of steroid hormones, thereby altering their activity and solubility. The expression and activity of STS is increased in female mammalian tissues (including brain) during late pregnancy and into the postpartum period. STS-deficient human and mouse mothers (as a consequence of genetic mutation or acute pharmacological manipulation) show evidence for elevated psychopathology and abnormal behaviour respectively in the postpartum period. In mice, these behavioural effects can be partially normalised through administration of the antipsychotic ziprasidone. Methods:To explore the neurobiology underlying these postpartum behavioural effects, we compared whole brain gene expression by microarray in behaviourally-defined new mouse mothers acutely administered the STS inhibitor 667-Coumate (10mg/kg p.o.) or vehicle solution (n=12 per group); significant changes were followed-up with pathway analysis and quantitative polymerase chain reaction (qPCR). Finally, the effects of combined 667-Coumate and antipsychotic (ziprasidone) administration (0, 0.3 and 1.0mg/kg i.p.) on the brain expression of the most robustly differentially-expressed candidate genes was examined (n≥7 per group). Results: Surprisingly, no significant gene expression changes were detected between vehicle and 667-Coumate-treated brains at a False Discovery Rate (FDR) corrected p<0.1. 1,081 unique expression changes were detected at a less-stringent cut-off of p<0.05, just two top hits were verified by qPCR, and pathway analysis indicated a significant enrichment of genes involved in olfactory transduction (corrected p-value=1.8x10 -3 ). The expression of the two most robust differentially-expressed genes (Stoml3 and Cyp2g1) was not affected by ziprasidone administration. Conclusions:Behavioural abnormalities in new mothers in the postpartum period elicited as a result of STS deficiency are likely to be the culmination of many small gene expression changes. Our data are consistent with the idea that olfactory function is key to postpartum maternal behaviour in mice, and suggest that aberrant expression of olfactory system genes may partially underlie abnormal maternal behaviour in STS-deficient women.

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Genetic and neuroendocrine regulation of the postpartum brain

Cited by 32 publications

References 162 publications

AMPK: Potential Therapeutic Target for Ischemic Stroke

AMPK: Potential Therapeutic Target for Ischemic Stroke

Brain vasopressin signaling modulates aspects of maternal behavior in lactating rats

Brain gene expression in a novel mouse model of postpartum mood disorder

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