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  1. Article ; Online: Na

    Salgado-Mozo, Sandra / Thirouin, Zahra S / Wyrosdic, Joshua C / García-Hernández, Ubaldo / Bourque, Charles W

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2023  Volume 43, Issue 49, Page(s) 8306–8316

    Abstract: ... ...

    Abstract The
    MeSH term(s) Animals ; Female ; Male ; Rats ; Hypernatremia/metabolism ; Oxytocin/metabolism ; Sodium/metabolism ; Supraoptic Nucleus/metabolism ; Vasopressins/metabolism ; Voltage-Gated Sodium Channels/metabolism ; Voltage-Gated Sodium Channels/physiology
    Chemical Substances Oxytocin (50-56-6) ; Sodium (9NEZ333N27) ; Vasopressins (11000-17-2) ; Scn7a protein, rat ; Voltage-Gated Sodium Channels
    Language English
    Publishing date 2023-12-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.1203-23.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1668: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: High dietary salt amplifies osmoresponsiveness in vasopressin-releasing neurons.

    Levi, David I / Wyrosdic, Joshua C / Hicks, Amirah-Iman / Andrade, Mary Ann / Toney, Glenn M / Prager-Khoutorsky, Masha / Bourque, Charles W

    Cell reports

    2021  Volume 34, Issue 11, Page(s) 108866

    Abstract: High dietary salt increases arterial pressure partly through activation of magnocellular neurosecretory cells ( ... ...

    Abstract High dietary salt increases arterial pressure partly through activation of magnocellular neurosecretory cells (MNC
    MeSH term(s) Angiotensin II ; Animals ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cytoskeleton/drug effects ; Cytoskeleton/metabolism ; Disease Models, Animal ; Excitatory Postsynaptic Potentials/drug effects ; Hypertension/pathology ; Male ; Mechanotransduction, Cellular/drug effects ; Neurons/drug effects ; Neurons/metabolism ; Osmosis ; Probability ; Rats, Wistar ; Sodium Chloride, Dietary/adverse effects ; Synapses/drug effects ; Synapses/metabolism ; Vasopressins/metabolism ; Rats
    Chemical Substances Sodium Chloride, Dietary ; Vasopressins (11000-17-2) ; Angiotensin II (11128-99-7)
    Language English
    Publishing date 2021-04-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.108866
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Trpv4 Mediates Hypotonic Inhibition of Central Osmosensory Neurons via Taurine Gliotransmission.

    Ciura, Sorana / Prager-Khoutorsky, Masha / Thirouin, Zahra S / Wyrosdic, Joshua C / Olson, James E / Liedtke, Wolfgang / Bourque, Charles W

    Cell reports

    2018  Volume 23, Issue 8, Page(s) 2245–2253

    Abstract: The maintenance of hydromineral homeostasis requires bidirectional detection of changes in extracellular fluid osmolality by primary osmosensory neurons (ONs) in the organum vasculosum laminae terminalis (OVLT). Hypertonicity excites ONs in part through ... ...

    Abstract The maintenance of hydromineral homeostasis requires bidirectional detection of changes in extracellular fluid osmolality by primary osmosensory neurons (ONs) in the organum vasculosum laminae terminalis (OVLT). Hypertonicity excites ONs in part through the mechanical activation of a variant transient receptor potential vanilloid-1 channel (dn-Trpv1). However, the mechanism by which local hypotonicity inhibits ONs in the OVLT remains unknown. Here, we show that hypotonicity can reduce the basal activity of dn-Trpv1 channels and hyperpolarize acutely isolated ONs. Surprisingly, we found that mice lacking dn-Trpv1 maintain normal inhibitory responses to hypotonicity when tested in situ. In the intact setting, hypotonicity inhibits ONs through a non-cell-autonomous mechanism that involves glial release of the glycine receptor agonist taurine through hypotonicity activated anion channels (HAAC) that are activated subsequent to Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Hypotonic Solutions/pharmacology ; Ion Channel Gating/drug effects ; Mice, Inbred C57BL ; Mice, Transgenic ; Neural Inhibition/drug effects ; Neuroglia/drug effects ; Neuroglia/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Osmolar Concentration ; Synaptic Transmission/drug effects ; TRPV Cation Channels/metabolism ; Taurine/pharmacology
    Chemical Substances Hypotonic Solutions ; TRPV Cation Channels ; TRPV1 protein, mouse ; Trpv4 protein, mouse ; Taurine (1EQV5MLY3D) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2018-05-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2018.04.090
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Peripubertal gonadal steroids are necessary for steroid-independent male sexual behavior in castrated B6D2F1 male mice.

    Templin, Jay Scott / Wyrosdic, Joshua C / David, Caroline D / Wyrosdic, Brianna N / Lapp, Hannah E / Bala, Andis / Bartlett, Alexander / Khan, Zara / Rokicki, Alicia / Park, Jin Ho

    Hormones and behavior

    2019  Volume 113, Page(s) 38–46

    Abstract: Gonadal steroids play an integral role in male sexual behavior, and in most rodent models, this relationship is tightly coupled. However, many other species, including humans, continue to demonstrate male sex behavior in the absence of gonadal steroids, ... ...

    Abstract Gonadal steroids play an integral role in male sexual behavior, and in most rodent models, this relationship is tightly coupled. However, many other species, including humans, continue to demonstrate male sex behavior in the absence of gonadal steroids, and the mechanisms that regulate steroid-independent male sex behavior are not well understood. Approximately 30% of castrated male B6D2F1 hybrid mice display male sex behavior many months after castration, allowing for the investigation of individual variation in steroidal regulation of male sex behavior. During both the perinatal and peripubertal periods of development, the organizational effects of gonadal steroids on sexual differentiation of the neural circuits controlling male sex behavior are well-documented. Several factors can alter the normal range of gonadal steroids or their receptors which may lead to the disruption of the normal processes of masculinization and defeminization. It is unknown whether the organizational effects of gonadal hormones during puberty are necessary for steroid-independent male sex behavior. However, gonadal steroids during puberty were not necessary for either testosterone or estradiol to activate male sex behavior in adulthood. Furthermore, activation of male sex behavior was initiated sooner in hybrid male mice castrated prior to puberty that were administered estradiol in adulthood compared to those that were provided testosterone. The underlying mechanisms by which gonadal hormones, during both the perinatal and peripubertal developmental periods of sexual differentiation, organize the normal maturation of neural circuitry that regulates steroid-independent male sex behavior in adult castrated B6D2F1 male mice warrants further investigation.
    MeSH term(s) Animals ; Estradiol/pharmacology ; Female ; Gonadal Steroid Hormones/pharmacology ; Gonadal Steroid Hormones/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Orchiectomy ; Sex Differentiation/drug effects ; Sexual Behavior, Animal/drug effects ; Sexual Maturation/drug effects ; Sexual Maturation/physiology ; Steroids/pharmacology ; Steroids/physiology ; Testosterone/pharmacology ; Testosterone/physiology
    Chemical Substances Gonadal Steroid Hormones ; Steroids ; Testosterone (3XMK78S47O) ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2019-05-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 214409-8
    ISSN 1095-6867 ; 0018-506X
    ISSN (online) 1095-6867
    ISSN 0018-506X
    DOI 10.1016/j.yhbeh.2019.04.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 693: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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