Developmental pathway genes and neural plasticity underlying emotional learning and stress-related disorders.

The manipulation of neural plasticity as a means of intervening in the onset and progression of stress-related disorders retains its appeal for many researchers, despite our limited success in translating such interventions from the laboratory to the clinic. Given the challenges of identifying individual genetic variants that confer increased risk for illnesses like depression and post-traumatic stress disorder, some have turned their attention instead to focusing on so-called "master regulators" of plasticity that may provide a means of controlling these potentially impaired processes in psychiatric illnesses. The mammalian homolog of (TLX), Wnt, and the homeoprotein Otx2 have all been proposed to constitute master regulators of different forms of plasticity which have, in turn, each been implicated in learning and stress-related disorders.

WITHDRAWN: Global and site-specific changes in 5-methylcytosine and 5-hydroxymethylcytosine after extended post-mortem interval.

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Global and Site-Specific Changes in 5-Methylcytosine and 5-Hydroxymethylcytosine after Extended Post-mortem Interval.

There has been a growing interest in the study of epigenetic mechanisms to elucidate the molecular bases of human brain-related diseases and disorders. Frequently, researchers utilize post-mortem tissue with the assumption that post-mortem tissue decay has little or no effect on epigenetic marks. Although previous studies show no effect of post-mortem interval on certain epigenetic marks, no such research has been performed on cytosine modifications.

Effects of postmortem interval on biomolecule integrity in the brain.

Postmortem brain research is invaluable to the study of neurologic and neuropsychiatric disorders, including Alzheimer disease, schizophrenia, and major depression. A major confounder in molecular studies using human brain tissue is postmortem interval (i.e.

Developmental hippocampal neuroplasticity in a model of nicotine replacement therapy during pregnancy and breastfeeding.

Rationale: The influence of developmental nicotine exposure on the brain represents an important health topic in light of the popularity of nicotine replacement therapy (NRT) as a smoking cessation method during pregnancy.

Objectives: In this study, we used a model of NRT during pregnancy and breastfeeding to explore the consequences of chronic developmental nicotine exposure on cerebral neuroplasticity in the offspring. We focused on two dynamic lifelong phenomena in the dentate gyrus (DG) of the hippocampus that are highly sensitive to the environment: granule cell neurogenesis and long-term potentiation (LTP).

Callosal oligodendrocyte number in postpartum Sprague-Dawley rats.

Prolactin (PRL), an anterior pituitary hormone with neurogenic properties associated with pregnancy, has been implicated in oligodendrocyte proliferation during gestation, contributing to increased myelination in the maternal brain. However, PRL is elevated during lactation as well, suggesting that the postpartum (PP) period may contribute to additional gliogenesis in lactating females. In the present study, we assessed oligodendrocyte number in the corpus callosum (CC) of female Sprague-Dawley rats near the end of gestation, and at two weeks postpartum in both lactating and non-lactating dams, and in virgins.