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  • 1
    In: Drug Development Research, Wiley, Vol. 66, No. 2 ( 2005-10), p. 142-149
    Abstract: High‐level estradiol enhances cell proliferation in the dentate gyrus of adult female rats within 4 h of administration and then suppresses cell proliferation within 48 h via an adrenal steroid‐dependent mechanism (Ormerod et al., [2003b] J Neurobiol 55:247–260). Here, we investigate whether the estradiol‐induced enhancement in progenitor cell proliferation is mediated through estrogen receptors (ERSs) using the selective ER antagonist ICI 182,780 (ICI). Ovariectomized Sprague‐Dawley rats were given two subcutaneous injections of either vehicle + vehicle (VEH; 0.1 ml sesame oil); VEH+ICI (500 µg); estradiol benzoate (EB; 10 µg)+VEH; or EB +ICI. The cell synthesis marker, 5‐bromo‐2′‐deoxyuridine (200 mg/kg) was administered 4 h later. Animals were perfused 24 h after BrdU injection and cell proliferation was assessed following immunohistochemical processing of the tissue. Relative to VEH, EB increased cell proliferation by approximately 50%. This EB‐induced increase was partially blocked by ICI 182,780 treatment, and ICI 182,780 treatment alone enhanced cell proliferation. Our results demonstrate that estradiol enhances cell proliferation in the dentate gyrus of adult female rats by activating estrogen receptors. Drug Dev. Res. 66:142–149, 2006. © 2006 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0272-4391 , 1098-2299
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 1500191-X
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2004
    In:  Journal of Neuroscience Research Vol. 76, No. 2 ( 2004-04-15), p. 216-222
    In: Journal of Neuroscience Research, Wiley, Vol. 76, No. 2 ( 2004-04-15), p. 216-222
    Type of Medium: Online Resource
    ISSN: 0360-4012 , 1097-4547
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2004
    detail.hit.zdb_id: 1474904-X
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  • 3
    Online Resource
    Online Resource
    Wiley ; 2007
    In:  Developmental Neurobiology Vol. 67, No. 10 ( 2007-09-01), p. 1321-1333
    In: Developmental Neurobiology, Wiley, Vol. 67, No. 10 ( 2007-09-01), p. 1321-1333
    Type of Medium: Online Resource
    ISSN: 1932-8451 , 1932-846X
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2266191-8
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  • 4
    Online Resource
    Online Resource
    Wiley ; 2006
    In:  Hippocampus Vol. 16, No. 3 ( 2006-01), p. 225-232
    In: Hippocampus, Wiley, Vol. 16, No. 3 ( 2006-01), p. 225-232
    Abstract: Gonadal hormones modulate neurogenesis in the dentate gyrus (DG) of adult rodents in complex ways. Estradiol, the most potent estrogen, initially enhances and subsequently suppresses cell proliferation in the dentate gryus of adult female rodents. Much less is known about how estradiol modulates neurogenesis in the adult male rodent; however, recent evidence suggests that estradiol may have a moderate effect on cell proliferation but enhances cell survival in the DG of newly synthesized cells but only when estradiol is administered during a specific stage in the cell maturation cycle in the adult male rodent. Testosterone likely plays a role in adult neurogenesis, although there have been no direct studies to address this. However, pilot studies from our laboratory suggest that testosterone up‐regulates cell survival but not cell proliferation in the DG of adult male rats. Progesterone appears to attenuate the estradiol‐induced enhancement of cell proliferation. Neurosteroids such as allopregnalone decrease neurogenesis in adult rodents, while pregnancy and motherhood differentially regulate adult neurogenesis in the adult female rodent. Very few studies have investigated the effects of gonadal hormones on male rodents; however, studies have indicated that there is a gender difference in the response to hormone‐regulated hippocampal neurogenesis in the adult. Clearly, more work needs to be done to elucidate the effects of gonadal hormones on neurogenesis in the DG of both male and female rodents. © 2006 Wiley‐Liss Inc.
    Type of Medium: Online Resource
    ISSN: 1050-9631 , 1098-1063
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 1498049-6
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  • 5
    In: Hippocampus, Wiley, Vol. 26, No. 1 ( 2016-01), p. 87-101
    Type of Medium: Online Resource
    ISSN: 1050-9631
    Language: English
    Publisher: Wiley
    Publication Date: 2016
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  • 6
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    Online Resource
    Wiley ; 2017
    In:  Journal of Neuroscience Research Vol. 95, No. 1-2 ( 2017-01-02), p. 50-64
    In: Journal of Neuroscience Research, Wiley, Vol. 95, No. 1-2 ( 2017-01-02), p. 50-64
    Abstract: Sex differences exist in the vulnerability, incidence, manifestation, and treatment of numerous neurological and psychiatric diseases. Despite this observation prominent in the literature, little consideration has been given to possible sex differences in outcome in both preclinical and clinical research. This Mini‐Review highlights evidence supporting why studying sex differences matter for advances in brain health as well as improving treatment for neurological and psychiatric disease. Additionally, we discuss some statistical and methodological considerations in evaluating sex differences as well as how differences in the physiology of the sexes can contribute to sex difference in disease incidence and manifestation. Furthermore, we review literature demonstrating that the reproductive experience in the female can render the female brain differentially vulnerable to disease across age. Finally, we discuss how genes interact with sex to influence disease risk and treatment and argue that sex must be considered in precision medicine. Together the evidence reviewed here supports the inclusion of males and females at all levels of neuroscience research. © 2016 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0360-4012 , 1097-4547
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 1474904-X
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  • 7
    Online Resource
    Online Resource
    Wiley ; 2006
    In:  Journal of Neurobiology Vol. 66, No. 1 ( 2006-01), p. 71-81
    In: Journal of Neurobiology, Wiley, Vol. 66, No. 1 ( 2006-01), p. 71-81
    Type of Medium: Online Resource
    ISSN: 0022-3034 , 1097-4695
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 1474900-2
    detail.hit.zdb_id: 2266191-8
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  • 8
    Online Resource
    Online Resource
    Wiley ; 2010
    In:  Hippocampus Vol. 20, No. 7 ( 2010-07), p. 866-876
    In: Hippocampus, Wiley, Vol. 20, No. 7 ( 2010-07), p. 866-876
    Abstract: Adult neurogenesis continues throughout life in the mammalian hippocampus. The precise function of the adult generated neurons remains uncertain although there is growing evidence that they are involved in hippocampus‐dependent learning and memory. Training rats on a hidden platform version of the Morris water task has been shown to increase or decrease the survival of newly produced cells in the dentate gyrus (DG) compared to training on a visible platform version. Here we investigated whether the difficulty of the task is related to the degree or direction of the change in neurogenesis. We trained rats on either a visible platform version of the Morris water task or one of three different hidden platform paradigms: four training trials per session version, two training trials per session, and reduced‐cue (a version in which the majority of the distal cues were removed from the room). BrdU was administered 6 days prior to training and rats were perfused 24 h after the last training session. As expected, training on the four trial hidden platform version increased cell survival compared to training on the visible platform version. However, training on the more difficult reduced‐cue hidden platform version resulted in a decrease in cell survival. Rats that received fewer trials per session did not differ in terms of cell survival in comparison to rats trained on the visible platform version. These findings demonstrate that altering the difficulty of the spatial task has an impact on the corresponding change in cell survival. The lack of obvious distal cues likely changed the strategy used by the rats to determine the location of the platform and resulted in a decrease, instead of an increase in cell survival in the hippocampus. In conclusion, different types of hippocampus‐dependent learning can differentially impact cell survival. © 2009 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 1050-9631 , 1098-1063
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2010
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  • 9
    In: Hippocampus, Wiley, Vol. 21, No. 11 ( 2011-11), p. 1216-1227
    Abstract: Previous studies have shown a relationship between adversity in adolescence and health outcomes in adulthood in a sex‐specific manner. Adolescence is characterized by major changes in stress‐responsive regions of the brain, including the hippocampus, the site of ongoing neurogenesis throughout the lifespan. Prepubertal male and female rats exhibit different acute reactions to chronic stress compared to adults, but less is known about whether these stress‐induced changes persist into adulthood. Therefore, in this study, we investigated the effects of chronic, intermittent stress during adolescence on basal corticosterone levels, dentate gyrus (DG) volume, and neurogenesis in the hippocampus of adult male and female Sprague‐Dawley rats. Adolescent male and female rats were either restrained for 1 h every other day for 3 weeks from postnatal days (PDs) 30–52 at unpredictable times or left undisturbed. All rats received a single injection of bromodeoxyuridine (BrdU; 200 mg/kg) in adulthood on PD70 and were perfused 3 weeks later. Brains were processed for Ki67 (endogenous marker of cell proliferation) and BrdU (to estimate effects on cell survival). In addition, blood samples were taken during the restraint stress period and in adulthood. Results show that males and females exhibit different corticosterone responses to chronic stress during adolescence and that only adult female rats exposed to stress during adolescence show higher basal corticosterone levels compared to nonstressed controls. Furthermore, stressed females showed a reduced number of proliferating and surviving cells in the DG in adulthood compared to nonstressed same‐sex controls. The majority of BrdU‐labeled cells were co‐labeled with NeuN, an endogenous marker of mature neurons, indicating that neurogenesis was decreased in the DG of adult female rats that had undergone chronic restraint stress in adolescence. Although male rats were more responsive to the chronic stress as adolescents showing higher corticosterone levels and reduced body weight, as adults they showed a slight increase in cellsurvival and no effect of adolescent stress on basal corticosterone levels. These results suggest that stress during adolescence can have effects on hypothalamic‐pituitary‐adrenal axis function and hippocampus plasticity in adulthood, particularly in female rats. ©2010 Wiley‐Liss,Inc.
    Type of Medium: Online Resource
    ISSN: 1050-9631 , 1098-1063
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2011
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  • 10
    In: Hippocampus, Wiley, Vol. 24, No. 3 ( 2014-03), p. 280-292
    Abstract: Cannabinoid exposure during adolescence has adverse effects on neuroplasticity, emotional behavior, cognition, and reward sensitivity in adult rats. We investigated whether escalating doses of the cannabinoid receptor 1 (CB 1 R) agonist, HU‐210, in adolescence would affect adult hippocampal neurogenesis and behavioral processes putatively modulated by hippocampal neurogenesis, in adult male and female Sprague‐Dawley rats. Escalating doses of HU‐210 (25, 50, and 100 µg/kg), or vehicle were administered from postnatal day (PND) 35 to 46. Animals were left undisturbed until PND 70, when they were treated with 5‐bromo‐2‐deoxyuridine (BrdU; 200 mg/kg) and perfused 21 days later to examine density of BrdU‐ir and BrdU/NeuN cells in the dentate gyrus. In another cohort, hypothalamic‐pituitary‐adrenal (HPA) axis reactivity to an acute restraint stress (30 min; PND 75) and behavioral sensitization to d‐amphetamine sulfate (1‐2 mg/kg; PND 105‐134) were assessed in adulthood. Adolescent HU‐210 administration suppressed the density of BrdU‐ir cells in the dentate gyrus in adult male, but not adult female rats. Adolescent HU‐210 administration also induced significantly higher peak corticosterone levels and reminiscent of the changes in neurogenesis, this effect was more pronounced in adult males than females. However, adolescent cannabinoid treatment resulted in significantly higher stereotypy scores in adult female, but not male, rats. Thus, adolescent CB 1 R activation suppressed hippocampal neurogenesis and increased stress responsivity in adult males, but not females, and enhanced amphetamine sensitization in adult female, but not male, rats. Taken together, increased CB 1 R activation during adolescence results in sex‐dependent, long‐term, changes to hippocampal structure and function, an effect that may shed light on differing vulnerabilities to developing disorders following adolescent cannabinoid exposure, based on sex. © 2013 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 1050-9631 , 1098-1063
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2014
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