Comparing rat’s to human’s age: How old is my rat in people years?
(Impact Factor: 2.93).
07/2005; 21(6):775-7. DOI: 10.1016/j.nut.2005.04.002
Available from: Alexandra N Garcia
- "Animals were randomly assigned to one of eight treatment groups as illustrated in Fig. 1 to test different timings and durations of hormone treatment based on those used in the WHI, in which the women experienced an average 12-year delay in treatment relative to the last menstrual period. We calculated based upon the rats' life cycle compared to humans, that 3 months to an adult rat is equal to about 5 years in a woman (Sengupta, 2013; Quinn, 2005). Capsules containing either 100% cholesterol (Veh) or 5% 17b- estradiol/95% cholesterol (E 2 ) were implanted subcutaneously between the shoulder blades at the time of surgery. "
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ABSTRACT: The current study tested the "critical window" hypothesis of menopause that postulates that the timing and duration of hormone treatment determine their potential outcomes. Our focus was genes in the rat hypothalamus involved in social and affiliative behaviors that change with aging and/or estradiol (E2): Avp, Avpr1a, Oxt, Oxtr, and Esr2 in the paraventricular nucleus (PVN) and supraoptic nucleus (SON). Rats were reproductively mature or aging adults, ovariectomized, given E2 or vehicle treatment of different durations, with or without a post-OVX delay. Our hypothesis was that age-related changes in gene expression are mitigated by E2 treatments. Contrary to this, PVN Oxtr increased with E2, and Avpr1a increased with age. In the SON, Avpr1a increased with age, Oxtr with age and timing, and Avp was by duration. Thus, chronological age and E2 have independent actions on gene expression, with the "critical window" hypothesis supported by the observed timing and duration effects.
Molecular and Cellular Endocrinology 10/2015; DOI:10.1016/j.mce.2015.10.004 · 4.41 Impact Factor
Available from: Maya Frankfurt
- "Following a one-week acclimation period during which animals were allowed to adjust to the new housing conditions, male and female adolescent subjects (Andreollo et al., 2012; Kwekel et al., 2010; Quinn, 2005), now aged 6 weeks, were randomly assigned to either a control (vehicle only) or experimental group (BPA exposed). BPA (N99% purity grade) was obtained from Sigma-Aldrich Corp (St. "
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ABSTRACT: We have previously demonstrated that adolescent exposure of rats to bisphenol-A (BPA), an environmental endocrine disrupter, increases anxiety, impairs spatial memory, and decreases dendritic spine density in the CA1 region of the hippocampus (CA1) and medial prefrontal cortex (mPFC) when measured in adolescence in both sexes. The present study examined whether the behavioral and morphological alterations following BPA exposure during adolescent development are maintained into adulthood. Male and female, adolescent rats received BPA, 40μg/kg/bodyweight, or control treatments for one week. In adulthood, subjects were tested for anxiety and locomotor activity, spatial memory, non-spatial visual memory, and sucrose preference. Additionally, stress-induced serum corticosterone levels and dendritic spine density in the mPFC and CA1 were measured. BPA-treated males, but not females, had decreased arm visits on the elevated plus maze, but there was no effect on anxiety. Non-spatial memory, object recognition, was also decreased in BPA treated males, but not females. BPA exposure did not alter spatial memory, object placement, but decreased exploration during the tasks in both sexes. No significant group differences in sucrose preference or serum corticosterone levels in response to a stress challenge were found. However, BPA exposure, regardless of sex, significantly decreased spine density of both apical and basal dendrites on pyramidal cells in CA1 but had no effect in the mPFC. Current data are discussed in relation to BPA dependent changes, which were present during adolescence and did, or did not, endure into adulthood. Overall, adolescent BPA exposure, below the current reference safe daily limit set by the U.S.E.P.A., leads to alterations in some behaviors and neuronal morphology that endure into adulthood.
Copyright © 2014. Published by Elsevier Inc.
Hormones and Behavior 12/2014; 69. DOI:10.1016/j.yhbeh.2014.12.007 · 4.63 Impact Factor
Available from: Adi Cymerblit-Sabba
- "These observations are supported by human studies, demonstrating the 'programming' effects of stress in early life on the HPA axis and the brain (Barker, 1991), and further presented in adult patients suffering from major depressive disorders who had experienced early life stress, and show persistent hyper activity of the HPA axis and of the autonomous nervous system, as well as increased sensitivity of these systems to stress (Heim et al., 2000a,b). Carefully considering the complex translation of rat to human lifespan (Quinn, 2005), together with the vigorous maturation which the brain undergoes during the transition period between childhood to adulthood (Sowell et al., 1999; Rubinow and Juraska, 2009; Avital et al., 2011), it seems that the available data supports the hypothesis that adolescence is a 'stress-sensitive' period (Andersen and Teicher, 2008; Leussis and Andersen, 2008). However, it has been also suggested that the development of emotionality and its underlying neural systems, remain highly plastic during the juvenile and pubescence periods (Holmes et al., 2005; Holder and Blaustein, 2014). "
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ABSTRACT: The exposure to stress at different developmental time points has long been postulated to have a crucial impact on various brain structures involved in mental disorders. The long-term specific effects seem to emerge as a function of timing and duration of the exposure to stress, as well as the characteristics of the stressor. Previous studies have addressed this issue with an effort to describe a single "hyper-sensitive" time point, and have led to disagreement on a particular sensitive period for stress exposure. The primary aim of our study was to investigate the hypothesis that indeed there is a developmental stress risk window in male Wistar rats. We conducted a systematic mapping of the long-term effects of an acute stress protocol, applied both prenatal (gestational days 14-16) and postnatal (days 9-151), overall at 11 different time-points during development. Stress protocol consists of 3 days of either maternal separation (for rats at postnatal days 9-19) or exposure to the stressors forced swim, elevated plus maze and restraint (for both dams and males at postnatal days 24-151). Consequences in adulthood were measured by investigating the animals' behavior in both the open field and startle box, together with the physiological measure of corticosterone. We found both behaviorally and physiologically that the pubescence time points are the most vulnerable to stress compared to all other tested time points along the developmental trajectory. Carefully considering the comparison between rat and human age, our findings may imply the importance of childhood-to-adulthood transition, as a sensitive time-point which may exacerbate a predisposition for the development of stress-induced psychopathologies.
Copyright © 2014. Published by Elsevier Ltd.
Psychoneuroendocrinology 11/2014; 52C(1):168-175. DOI:10.1016/j.psyneuen.2014.11.012 · 4.94 Impact Factor
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