Effect of perinatal HDAC inhibitor administration on sexual differentiation of vasopressin innervation in the mouse brain

Elaine Murray, JL Fernandez, NG Forger, GJ De Vries

    Research output: Chapter in Book/Report/Conference proceedingConference contribution

    Abstract

    In most vertebrates studied, males have more vasopressin (VP) cells in the bed nucleus of the stria terminalis (BNST) and denser projections from these cells than do females. This sex difference is established perinatally and maintained in adulthood by steroid hormones. The mechanisms of hormone action, however, remain unknown. Previous studies have eliminated differential cell birth, migration, and cell death as likely factors, leaving cell phenotypic differentiation as the most likely mechanism. We hypothesized that hormones influence vasopressin expression through epigenetic mechanisms. We, therefore, manipulated the balance between histone acetylation and deacetylation by treating animals with the histone deacetylase inhibitor valproic acid (VPA) during a critical time for sexual differentiation. Males and females were given 50mg/kg VPA or saline on postnatal days 1 and 2. Animals were sacrificed in adulthood and their brains were processed for vasopressin immunoreactivity. As predicted, males had greater vasopressin innervation in the lateral septum than females. VPA treatment increased vasopressin in the lateral septum in females but had no effect in males, thereby reducing but not eliminating the sex difference. There was no effect of sex or VPA treatment on vasopressin immunoreactivity in the anterior paraventicular nucleus of the thalamus, which receives its innervation from the suprachiasmatic nucleus. These results suggest that histone acetylation contributes to the sexual differentiation of vasopressin expression.
    LanguageEnglish
    Title of host publicationUnknown Host Publication
    Number of pages1
    Publication statusPublished - 2009
    EventSociety for Neuroscience, 2009 - Chicago
    Duration: 1 Jan 2009 → …

    Conference

    ConferenceSociety for Neuroscience, 2009
    Period1/01/09 → …

    Fingerprint

    Sex Differentiation
    Histone Deacetylase Inhibitors
    Vasopressins
    Valproic Acid
    Brain
    Hormones
    Acetylation
    Sex Characteristics
    Histones
    Anterior Thalamic Nuclei
    Septal Nuclei
    Suprachiasmatic Nucleus
    Epigenomics
    Cell Movement
    Vertebrates
    Cell Differentiation
    Cell Death
    Steroids
    Parturition

    Cite this

    @inproceedings{bac60162a096451e8c59abc2babebcb1,
    title = "Effect of perinatal HDAC inhibitor administration on sexual differentiation of vasopressin innervation in the mouse brain",
    abstract = "In most vertebrates studied, males have more vasopressin (VP) cells in the bed nucleus of the stria terminalis (BNST) and denser projections from these cells than do females. This sex difference is established perinatally and maintained in adulthood by steroid hormones. The mechanisms of hormone action, however, remain unknown. Previous studies have eliminated differential cell birth, migration, and cell death as likely factors, leaving cell phenotypic differentiation as the most likely mechanism. We hypothesized that hormones influence vasopressin expression through epigenetic mechanisms. We, therefore, manipulated the balance between histone acetylation and deacetylation by treating animals with the histone deacetylase inhibitor valproic acid (VPA) during a critical time for sexual differentiation. Males and females were given 50mg/kg VPA or saline on postnatal days 1 and 2. Animals were sacrificed in adulthood and their brains were processed for vasopressin immunoreactivity. As predicted, males had greater vasopressin innervation in the lateral septum than females. VPA treatment increased vasopressin in the lateral septum in females but had no effect in males, thereby reducing but not eliminating the sex difference. There was no effect of sex or VPA treatment on vasopressin immunoreactivity in the anterior paraventicular nucleus of the thalamus, which receives its innervation from the suprachiasmatic nucleus. These results suggest that histone acetylation contributes to the sexual differentiation of vasopressin expression.",
    author = "Elaine Murray and JL Fernandez and NG Forger and {De Vries}, GJ",
    year = "2009",
    language = "English",
    booktitle = "Unknown Host Publication",

    }

    Murray, E, Fernandez, JL, Forger, NG & De Vries, GJ 2009, Effect of perinatal HDAC inhibitor administration on sexual differentiation of vasopressin innervation in the mouse brain. in Unknown Host Publication. Society for Neuroscience, 2009, 1/01/09.

    Effect of perinatal HDAC inhibitor administration on sexual differentiation of vasopressin innervation in the mouse brain. / Murray, Elaine; Fernandez, JL; Forger, NG; De Vries, GJ.

    Unknown Host Publication. 2009.

    Research output: Chapter in Book/Report/Conference proceedingConference contribution

    TY - GEN

    T1 - Effect of perinatal HDAC inhibitor administration on sexual differentiation of vasopressin innervation in the mouse brain

    AU - Murray, Elaine

    AU - Fernandez, JL

    AU - Forger, NG

    AU - De Vries, GJ

    PY - 2009

    Y1 - 2009

    N2 - In most vertebrates studied, males have more vasopressin (VP) cells in the bed nucleus of the stria terminalis (BNST) and denser projections from these cells than do females. This sex difference is established perinatally and maintained in adulthood by steroid hormones. The mechanisms of hormone action, however, remain unknown. Previous studies have eliminated differential cell birth, migration, and cell death as likely factors, leaving cell phenotypic differentiation as the most likely mechanism. We hypothesized that hormones influence vasopressin expression through epigenetic mechanisms. We, therefore, manipulated the balance between histone acetylation and deacetylation by treating animals with the histone deacetylase inhibitor valproic acid (VPA) during a critical time for sexual differentiation. Males and females were given 50mg/kg VPA or saline on postnatal days 1 and 2. Animals were sacrificed in adulthood and their brains were processed for vasopressin immunoreactivity. As predicted, males had greater vasopressin innervation in the lateral septum than females. VPA treatment increased vasopressin in the lateral septum in females but had no effect in males, thereby reducing but not eliminating the sex difference. There was no effect of sex or VPA treatment on vasopressin immunoreactivity in the anterior paraventicular nucleus of the thalamus, which receives its innervation from the suprachiasmatic nucleus. These results suggest that histone acetylation contributes to the sexual differentiation of vasopressin expression.

    AB - In most vertebrates studied, males have more vasopressin (VP) cells in the bed nucleus of the stria terminalis (BNST) and denser projections from these cells than do females. This sex difference is established perinatally and maintained in adulthood by steroid hormones. The mechanisms of hormone action, however, remain unknown. Previous studies have eliminated differential cell birth, migration, and cell death as likely factors, leaving cell phenotypic differentiation as the most likely mechanism. We hypothesized that hormones influence vasopressin expression through epigenetic mechanisms. We, therefore, manipulated the balance between histone acetylation and deacetylation by treating animals with the histone deacetylase inhibitor valproic acid (VPA) during a critical time for sexual differentiation. Males and females were given 50mg/kg VPA or saline on postnatal days 1 and 2. Animals were sacrificed in adulthood and their brains were processed for vasopressin immunoreactivity. As predicted, males had greater vasopressin innervation in the lateral septum than females. VPA treatment increased vasopressin in the lateral septum in females but had no effect in males, thereby reducing but not eliminating the sex difference. There was no effect of sex or VPA treatment on vasopressin immunoreactivity in the anterior paraventicular nucleus of the thalamus, which receives its innervation from the suprachiasmatic nucleus. These results suggest that histone acetylation contributes to the sexual differentiation of vasopressin expression.

    M3 - Conference contribution

    BT - Unknown Host Publication

    ER -