Cheryl L Sisk

Michigan State University, Ист-Лансинг, Michigan, United States

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Publications (115)437.49 Total impact

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    ABSTRACT: Binge eating is a key symptom of many eating disorders (e.g. binge eating disorder, bulimia nervosa, anorexia nervosa binge/purge type), yet the neurobiological underpinnings of binge eating are poorly understood. The mesocorticolimbic reward circuit, including the nucleus accumbens and the medial prefrontal cortex, is likely involved because this circuit mediates the hedonic value and incentive salience of palatable foods (PF). Here we tested the hypothesis that higher propensity for binge eating is associated with a heightened response (i.e., Fos induction) of the nucleus accumbens and medial prefrontal cortex to PF, using an animal model that identifies binge eating prone (BEP) and binge eating resistant (BER) rats. Forty adult female Sprague-Dawley rats were given intermittent access to PF (high fat pellets) 3×/week for 3weeks. Based on a pattern of either consistently high or consistently low PF consumption across these feeding tests, 8 rats met criteria for categorization as BEP, and 11 rats met criteria for categorization as BER. One week after the final feeding test, BEP and BER rats were either exposed to PF in their home cages or were given no PF in their home cages for one hour prior to perfusion, leading to three experimental groups for the Fos analysis: BEPs given PF, BERs given PF, and a No PF control group. The total number of Fos-immunoreactive (Fos-ir) cells in the nucleus accumbens core and shell, and the cingulate, prelimbic, and infralimbic regions of the medial prefrontal cortex was estimated by stereological analysis. PF induced higher Fos expression in the nucleus accumbens shell and core and in the prelimbic and infralimbic cortex of BEP rats compared to No PF controls. Throughout the nucleus accumbens and medial prefrontal cortex, PF induced higher Fos expression in BEP than in BER rats, even after adjusting for differences in PF intake. Differences in the neural activation pattern between BEP and BER rats were more robust in prefrontal cortex than in nucleus accumbens. These data confirm that PF activates brain regions responsible for encoding the incentive salience and hedonic properties of PF, and suggest that binge eating proneness is associated with enhanced responses to PF in brain regions that exert executive control over food reward.
    Full-text · Article · Oct 2015 · Physiology & Behavior
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    ABSTRACT: Previous studies have shown significant within-person changes in binge eating and emotional eating across the menstrual cycle, with substantial increases in both phenotypes during post-ovulation. Increases in both estradiol and progesterone levels appear to account for these changes in phenotypic risk, possibly via increases in genetic effects. However, to date, no study has examined changes in genetic risk for binge phenotypes (or any other phenotype) across the menstrual cycle. The goal of the present study was to examine within-person changes in genetic risk for emotional eating scores across the menstrual cycle. Participants were 230 female twin pairs (460 twins) from the Michigan State University Twin Registry who completed daily measures of emotional eating for 45 consecutive days. Menstrual cycle phase was coded based on dates of menstrual bleeding and daily ovarian hormone levels. Findings revealed important shifts in genetic and environmental influences, where estimates of genetic influences were two times higher in post- as compared with pre-ovulation. Surprisingly, pre-ovulation was marked by a predominance of environmental influences, including shared environmental effects which have not been previously detected for binge eating phenotypes in adulthood. Our study was the first to examine within-person shifts in genetic and environmental influences on a behavioral phenotype across the menstrual cycle. Results highlight a potentially critical role for these shifts in risk for emotional eating across the menstrual cycle and underscore the need for additional, large-scale studies to identify the genetic and environmental factors contributing to menstrual cycle effects.
    Full-text · Article · Jul 2015 · Psychological Medicine
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    ABSTRACT: Objective Negative urgency (NU; tendency to act impulsively when experiencing negative emotions) is a risk factor for binge eating, although few studies have examined interviewer-assessed objective binge episodes (OBEs). Moreover, research has not investigated how NU relates to the core components of OBEs: loss of control (LOC) eating and objective overeating (OO). Understanding the relationship between NU and these core components will enhance etiologic models of eating disorder development. Thus, the current study examined the associations between NU, OBEs, and the components of OBEs by comparing levels of NU in women with OBEs, LOC eating only, and OO only to women with no pathological eating.Method Participants were 612 women who endorsed lifetime OBEs (5.4%), LOC eating outside of OBEs (5.7%), OO only (2.8%), or none of these eating episodes (85.9%).ResultsWomen with OBEs, LOC only, and OO only had significantly higher levels of NU than women without these episodes, suggesting that NU is associated with both the LOC and OO components of OBEs.DiscussionNU relates to the spectrum of pathology present in women with OBEs. Future research should examine the mechanisms underlying these associations, including impaired behavioral/psychological control and/or increased reward sensitivity in response to negative affect. © 2015 Wiley Periodicals, Inc.© 2015 Wiley Periodicals, Inc (Int J Eat Disord 2015).
    No preview · Article · Apr 2015 · International Journal of Eating Disorders
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    ABSTRACT: Prenatal testosterone exposure may be protective against disordered eating. However, prior studies have produced mixed results. Developmental differences in prenatal testosterone's protective effects on disordered eating may explain these discrepancies. Indeed, studies have differed in the age of participants assessed, with data supporting prenatal testosterone effects on disordered eating in early adolescent and young adult samples but not in late adolescence. The present studies are the first to investigate age differences in prenatal testosterone's protective effects on disordered eating. Two indirect markers of higher prenatal testosterone were examined: (a) lower finger-length ratios (Study 1: index [2D]/ring [4D] finger [2D:4D]) and (b) lower disordered eating in female s from opposite-sex twin pairs (who are thought to be exposed to higher prenatal testosterone from their male co-twin) relative to female controls (Study 2). Participants were twins from the Michigan State University Twin Registry (Study 1: n = 409; Study 2: n = 1,538) in early adolescence, late adolescence, or young adulthood. Disordered eating was assessed with well-validated questionnaires. Finger-length ratios were measured from hand scans, using electronic computer calipers. Findings were consistent across both studies. Higher prenatal testosterone (lower 2D:4D; females from opposite-sex twin pairs vs. controls) predicted lower disordered eating in early adolescence and young adulthood only. Prenatal testosterone-disordered eating associations were not observed during late adolescence. Results point to the possibility of developmental windows of expression for prenatal testosterone's protective effects on disordered eating and suggest that prior discrepant results may reflect age differences across samples. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
    No preview · Article · Feb 2015 · Behavioral Neuroscience
  • Cheryl L. Sisk
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    ABSTRACT: Sexual differentiation of the nervous system and behavior occurs through organizational effects of gonadal hormones acting during early neural development and again during puberty. In rodents, a transient elevation in testosterone around the time of birth masculinizes and defeminizes the male brain, creating structural sexual dimorphisms and programming sex-typical responses to gonadal hormones in adulthood. A second wave of sexual differentiation occurs when levels of gonadal hormones are elevated at the time of puberty. At this time, both testicular and ovarian hormones further masculinize and feminize the male and female brain, respectively, fine-tuning sex differences in adult behavior. To test the hypothesis that the peripubertal period is a sensitive period for hormone-dependent sexual differentiation that is separate and distinct from the perinatal period, exposure to testosterone was experimentally manipulated in male Syrian hamsters to occur either prepubertally, during puberty, or in young adulthood. This experiment revealed that the perinatal and peripubertal periods of masculinization of male sexual behavior are not two separate critical periods of sensitivity to organizing effects of testosterone. Instead, the two periods of masculinization are driven by the two naturally occurring elevations in gonadal hormones. To explore possible neural mechanisms of peripubertal organizational effects of gonadal hormones, cell birthdating experiments in male and female rats revealed sex differences in the addition of new cells, including both neurons and glia, to sexually dimorphic cell groups in the hypothalamus and medial amygdala. These sex differences in cell addition were positively correlated with sex differences in the volume of these cell groups. Prepubertal gonadectomy abolished sex differences in the pubertal addition of new cells. These experiments provide evidence that gonadal hormone-dependent sex differences in pubertal cytogenesis contribute to the establishment or maintenance of sexual dimorphisms in the adult brain. The transition from childhood to adulthood begins with the onset of puberty and the ensuing rise in sex steroid hormones, and it is completed by the end of adolescence. This period of development comprises extraordinary gain of function: individuals acquire the capacity to procreate, function independently within their social realm, and provide for themselves and their offspring. The metamorphosis of behavior is the product of a metamorphosis of underlying neural circuits, which necessarily occurs along different trajectories in females and males. In fact, adolescence can be regarded as a period of further sexual differentiation of brain and behavior, which is mediated in part by the actions of sex steroid hormones in the brain. This paper highlights research from my laboratory that has uncovered roles for gonadal hormones in shaping sex-specific behavioral and brain development during puberty and adolescence. I will first review experiments that establish that testicular hormones, acting during puberty, organize neural circuits underlying male social behaviors. Next I will present evidence that hormonal regulation of pubertal neuro- and gliogenesis is a potential mechanism for the establishment or maintenance of structural sex differences in the brain during adolescence.
    No preview · Article · Jan 2015 · Research and Perspectives in Endocrine Interactions
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    ABSTRACT: Objective: Mean-levels of thin-ideal internalization increase during adolescence and pubertal development, but it is unknown whether these phenotypic changes correspond to developmental changes in etiological (i.e., genetic and environmental) risk. Given the limited knowledge on risk for thin-ideal internalization, research is needed to guide the identification of specific types of risk factors during critical developmental periods. The present twin study examined genetic and environmental influences on thin-ideal internalization across adolescent and pubertal development. Method: Participants were 1,064 female twins (ages 8-25 years) from the Michigan State University Twin Registry. Thin-ideal internalization and pubertal development were assessed using self-report questionnaires. Twin moderation models were used to examine if age and/or pubertal development moderate genetic and environmental influences on thin-ideal internalization. Results: Phenotypic analyses indicated significant increases in thin-ideal internalization across age and pubertal development. Twin models suggested no significant differences in etiologic effects across development. Nonshared environmental influences were most important in the etiology of thin-ideal internalization, with genetic, shared environmental, and nonshared environmental accounting for approximately 8%, 15%, and 72%, respectively, of the total variance. Discussion: Despite mean-level increases in thin-ideal internalization across development, the relative influence of genetic versus environmental risk did not differ significantly across age or pubertal groups. The majority of variance in thin-ideal internalization was accounted for by environmental factors, suggesting that mean-level increases in thin-ideal internalization may reflect increases in the magnitude/strength of environmental risk across this period. Replication is needed, particularly with longitudinal designs that assess thin-ideal internalization across key developmental phases.
    No preview · Article · Nov 2014 · International Journal of Eating Disorders
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    ABSTRACT: Changes in ovarian hormones predict changes in emotional eating across the menstrual cycle. However, prior studies have not examined whether the nature of associations varies across dysregulated eating severity. The current study determined whether the strength and/or nature of hormone/dysregulated eating associations differ based on the presence of clinically diagnosed binge episodes (BEs). Participants included 28 women with BEs and 417 women without BEs who provided salivary hormone samples, ratings of emotional eating, and BE frequency for 45 days. Results revealed stronger associations between dysregulated eating and ovarian hormones in women with BEs as compared to women without BEs. The nature of associations also differed, as progesterone moderated the effects of lower estradiol levels on dysregulated eating in women with BEs only. Although hormone/dysregulated eating associations are present across the spectrum of pathology, the nature of associations may vary in ways that have implications for etiological models and treatment.
    Full-text · Article · Sep 2014
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    ABSTRACT: Adolescence involves shifts in social behaviors, behavioral flexibility, and adaptive risk-taking that coincide with structural remodeling of the brain. We previously showed that new cells are added to brain regions associated with sexual behaviors, suggesting that cytogenesis may be a mechanism for acquiring adult-typical behaviors during adolescence. Whether pubertal cell addition occurs in brain regions associated with behavioral flexibility or motivation, and whether these patterns differ between pubertal and adult animals had not been determined. Therefore, we assessed patterns of cell proliferation or survival in the prefrontal cortex and nucleus accumbens. Pubertal and adult male rats were given injections of bromo-deoxyuridine (BrdU). To assess cell proliferation, half of the animals from each group were sacrificed 24 hours following the last injection. The remaining animals were sacrificed 30 days following the last injection to evaluate cell survival. Adult animals had significantly lower densities of BrdU-immunoreactive (ir) cells in the prefrontal cortex, irrespective of post-BrdU survival time, whereas in the nucleus accumbens, adult animals had a lower density of BrdU-ir cells at the short survival time, but the density was equivalent in pubertal and adult animals at the longer survival time. These data provide evidence that cell addition during puberty may contribute to the remodeling brain regions associated with behavioral flexibility and motivation, and this cell addition continues into adulthood, albeit at lower levels. Higher levels of cell proliferation or survival in younger animals may reflect a higher level of plasticity, possibly contributing to the dynamic remodeling of the pubertal brain. © 2013 Wiley Periodicals, Inc. Develop Neurobiol, 2013.
    No preview · Article · Jun 2014 · Developmental Neurobiology
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    ABSTRACT: Objective Previous research has shown that fluctuations in ovarian hormones (i.e., estradiol and progesterone) predict the changes in binge eating and emotional eating across the menstrual cycle. However, the extent to which other eating disorder symptoms fluctuate across the menstrual cycle and are influenced by ovarian hormones remains largely unknown. This study sought to examine whether the levels of weight preoccupation vary across the menstrual cycle and whether the changes in ovarian hormones and/or other factors (i.e., emotional eating and negative affect) account for menstrual cycle fluctuations in this eating disorder phenotype.Method For 45 consecutive days, 352 women (age, 15-25 years) provided daily ratings of weight preoccupation, negative affect, and emotional eating. Saliva samples were also collected on a daily basis and assayed for levels of estradiol and progesterone using enzyme immunoassay techniques.ResultsWeight preoccupation varied significantly across the menstrual cycle, with the highest levels in the premenstrual and menstrual phases. However, ovarian hormones did not account for within-person changes in weight preoccupation across the menstrual cycle. Instead, the most significant predictor of menstrual cycle changes in weight preoccupation was the change in emotional eating.DiscussionFluctuations in weight preoccupation across the menstrual cycle appear to be influenced primarily by emotional eating rather than ovarian hormones. Future research should continue to examine the relationships among ovarian hormones, weight preoccupation, emotional eating, and other core eating disorder symptoms (e.g., body dissatisfaction, compensatory behaviors) in an effort to more fully understand the role of these biological and behavioral factors for the full spectrum of eating pathology. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2014)
    No preview · Article · Jun 2014 · International Journal of Eating Disorders
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    ABSTRACT: A classical twin study was used to estimate the magnitude of genetic and environmental influences on four measurements of within-person variability: dominance flux, warmth flux, spin and pulse. Flux refers to the variability of an individual's interpersonal dominance and warmth. Spin measures changes in the tone of interpersonal styles and pulse measures changes in the intensity of interpersonal styles. Daily reports of interpersonal styles were collected from 494 same-sex female twins (142 monozygotic pairs and 105 dizygotic pairs) over 45 days. For dominance flux, warmth flux, and spin, genetic effects accounted for a larger proportion of variance (37%, 24%, and 30%, respectively) than shared environmental effects (14%, 13%, 0%, respectively), with the remaining variance due to the non-shared environment (62%, 50%, 70% respectively). Pulse appeared to be primarily influenced by the non-shared environment, although conclusions about the contribution of familial influences were difficult to draw from this study.
    Full-text · Article · Apr 2014 · Social Psychological and Personality Science
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    ABSTRACT: Binge eating is a significantly heritable phenotype, but efforts to detect specific risk genes have fallen short. Identification of animal strain differences in risk for binge eating could highlight genetic differences across individuals of the same species that can be exploited in future animal and molecular genetic research. The current study aimed to explore strain differences in risk for binge eating in Sprague-Dawley versus Wistar female rats using the Binge Eating Resistant/Binge Eating Prone model. A sample of male Sprague Dawley rats, a known low-risk group for binge eating, was included as a comparison group. A total of 83 rats (23 Wistar female, 30 Sprague-Dawley female, 30 Sprague-Dawley male) completed a protocol of intermittently administered, palatable food. Binge eating prone (BEP) and binge eating resistant (BER) rats were identified using a tertile approach. Sprague-Dawley female rats consumed the highest amount of palatable food and were more likely to be classified as BEP compared to Wistar female and Sprague-Dawley male rats. Wistar female rats were not significantly different from Sprague-Dawley male rats in their palatable food intake and tendency to be classified as BER rather than BEP. Sprague-Dawley female rats appear to be a particularly vulnerable genotype for binge eating. Comparisons between this group and others could help identify specific genetic/biological factors that differentiate it from lower risk groups. The reward system, linked to binge eating in humans, is a possible candidate to explore. Strain differences in the reward system could help increase understanding of individual differences in risk for binge eating in humans.
    No preview · Article · Jan 2014 · Physiology & Behavior
  • K M Culbert · S A Burt · C L Sisk · J T Nigg · K L Klump
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    ABSTRACT: Testosterone may be a biological factor that protects males against eating disorders. Elevated prenatal testosterone exposure is linked to lower levels of disordered eating symptoms, but effects emerge only after mid-puberty. Whether circulating levels of testosterone account for decreased risk for disordered eating in boys after mid-puberty is currently unknown; however, animal data support this possibility. In rodents, prenatal testosterone's masculinizing effects on sex-differentiated behaviors emerge during puberty when circulating levels of testosterone increase and 'activate' the expression of masculinized phenotypes. This study investigated whether higher levels of circulating testosterone predict lower levels of disordered eating symptoms in adolescent boys, and in particular whether effects are associated with advancing pubertal maturation. Participants were 213 male twins from the Michigan State University Twin Registry. The Minnesota Eating Behavior Survey and Eating Disorder Examination Questionnaire assessed several disordered eating symptoms. The Pubertal Development Scale assessed pubertal status. Afternoon saliva samples were assayed for testosterone using enzyme immunoassays. Consistent with animal data, higher levels of circulating testosterone predicted lower levels of disordered eating symptoms in adolescent boys and effects emerged with advancing puberty. Results were not accounted for by several important covariates, including age, adiposity, or mood/anxiety symptoms. Findings suggest that elevated circulating testosterone may be protective and underlie decreased risk for eating pathology in males during/after puberty, whereas lower levels of testosterone may increase risk and explain why some, albeit relatively few, males develop eating disorders.
    No preview · Article · Jan 2014 · Psychological Medicine
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    ABSTRACT: Animal studies indicate that gonadal hormones at puberty have an effect on the development of masculine and feminine traits. However, it is unknown whether similar processes occur in humans. We examined whether women with anorexia nervosa (AN), who often experience primary amenorrhea, exhibit attenuated feminization in their psychological characteristics in adulthood due to the decrease/absence of gonadal hormones at puberty. Women with AN were compared on a number of psychological characteristics using general linear models on the basis of the presence/absence of primary amenorrhea. Although women with primary amenorrhea exhibited lower anxiety scores than those without primary amenorrhea, in general, results did not provide evidence of attenuated feminization in women with AN with primary amenorrhea. Future research should utilize novel techniques and direct hormone measurement to explore the effects of pubertal gonadal hormones on masculine and feminine traits. Copyright © 2013 John Wiley & Sons, Ltd and Eating Disorders Association.
    Full-text · Article · Jan 2014 · European Eating Disorders Review
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    ABSTRACT: Previous research indicates that borderline personality disorder (BPD) is well conceptualized as a dimensional construct that can be represented using normal personality traits. A previous study successfully developed and validated a BPD measure embedded within a normal trait measure, the Minnesota Borderline Personality Disorder Scale (MBPD). The current study performed a further validation of the MBPD by examining its convergent validity, external correlates, and heritability in a sample of 429 female twins. The MBPD correlated strongly with the Structured Clinical Interview for DSM-IV Axis II Personality Disorders (SCID-II) screener for BPD and moderately with external correlates. Moreover, the MBPD and SCID-II screener exhibited very similar patterns of external correlations. Additionally, results indicated that the genetic and environmental influences on MBPD overlap with the genetic and environmental influences on the SCID-II screener, which suggests that these scales are measuring the same construct. These data provide further evidence for the construct validity of the MBPD. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
    Full-text · Article · Dec 2013 · Personality Disorders: Theory, Research, and Treatment
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    ABSTRACT: Objective Several efforts are underway to model binge eating in animals in order to advance neurobiological models of risk. However, knowledge of sex differences in these models is currently lacking. The goal of the present study was to examine sex differences in binge eating phenotypes using a well-established rodent model (i.e., the binge eating resistant/binge eating prone model). Method Thirty male and 30 female adult Sprague-Dawley rats were exposed to feeding tests consisting of intermittent access to palatable food (PF). Rats were then categorized as binge eating prone (BEP) based on the amount and consistency of PF consumption across tests. ResultsAcross multiple methods for BEP classification, rates of BEP phenotypes were two to six times higher in female than male rats. DiscussionFindings provide support for sex differences in rodent models of binge eating and highlight the promise of the BER/BEP model for understanding neurobiological mechanisms underlying sex differences in risk. (c) 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:729-736)
    No preview · Article · Nov 2013 · International Journal of Eating Disorders
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    ABSTRACT: Hormones exert powerful influences on mammalian nervous system development, particularly during developmental transitions associated with a change in reproductive state, including the perinatal period of sexual differentiation, puberty, pregnancy and lactation, and reproductive aging. This chapter focuses on the influences of gonadal steroid hormones, their sites and mechanisms of action, and behavioral outcomes during these reproductive transitions in mammals. The major emphasis of this chapter is on organizational influences of gonadal steroid hormones – that is, how early life exposures to hormones program neural and behavioral phenotypes expressed later in life. Organizational hormones, both endogenous and exogenous (such as endocrine disrupting chemicals), alter developmental trajectory, often irreversibly, and they program sensitivity and responsiveness of the nervous system to hormones during subsequent developmental transitions. Because hormonal influences during later periods of development depend to a large extent on hormonal events that occurred during earlier periods of development, the organizational effects of hormones are compounded over the lifespan. Thus, the overarching premise of this chapter is that hormonal life history underlies much of the complexity that characterizes individual differences in neural, behavioral, and other physiological responses, not only to endogenous hormones, but also to endocrine disruptors and hormonal therapies.
    Full-text · Chapter · Nov 2013
  • Margaret R Bell · Sarah H Meerts · Cheryl L Sisk
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    ABSTRACT: The interpretation of social cues must change during adolescence in order to promote appropriate social interactions in adulthood. For example, adult, but not juvenile, male Syrian hamsters find female pheromones contained in vaginal sections (VS) rewarding, and only adult hamsters engage in sexual behavior with a receptive female. We previously demonstrated that the rewarding value of VS is both testosterone- and dopamine-dependent. Additionally, VS induces Fos expression throughout the mesocorticolimbic circuit in adult but not juvenile hamsters. In this study, we determined whether or not treatment of juvenile male hamsters with testosterone is sufficient to promote adult-like neural responses to VS. Juvenile and adult male hamsters were gonadectomized and given empty or testosterone-filled subcutaneous capsules for one week. Hamsters were then exposed to either clean or VS-containing mineral oil on their nares, and brains were collected one hour later for immunohistochemistry to visualize Fos and tyrosine hydroxylase immunoreactive cells. Testosterone-treatment failed to promote adult-typical patterns of Fos expression in juvenile hamsters; indeed, in some brain regions, juveniles exposed to VS expressed less Fos compared to age-matched controls while, as expected, adults exposed to VS expressed greater Fos compared to age-matched controls. Age-related changes in tyrosine-hydroxylase expression were also observed. These data indicate that testosterone cannot activate the adult-typical pattern of Fos expression in response to female social cues in prepubertal males, and that additional neural maturation during adolescence is required for adult-typical mesocorticolimbic responses to female pheromones. © 2013 Wiley Periodicals, Inc. Develop Neurobiol, 2013.
    No preview · Article · Sep 2013 · Developmental Neurobiology
  • Cheryl L Sisk · Sheri A Berenbaum

    No preview · Article · Jul 2013 · Hormones and Behavior
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    Janice M Juraska · Cheryl L Sisk · Lydia L Doncarlos
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    ABSTRACT: This article is part of a Special Issue "Puberty and Adolescence". Sexual differentiation is the process by which the nervous system becomes structurally and functionally dissimilar in females and males. In mammals, this process has been thought to occur during prenatal and early postnatal development, when a transient increase in testosterone secretion masculinizes and defeminizes the developing male nervous system. Decades of research have led to the views that structural sexual dimorphisms created during perinatal development are passively maintained throughout life, and that ovarian hormones do not play an active role in feminization of the nervous system. Furthermore, perinatal testosterone was thought to determine sex differences in neuron number by regulating cell death and cell survival, and not by regulating cell proliferation. As investigations of neural development during adolescence became more prominent in the late 20th century and revealed the extent of brain remodeling during this time, each of these tenets has been challenged and modified. Here we review evidence from the animal literature that 1) the brain is further sexually differentiated during puberty and adolescence; 2) ovarian hormones play an active role in the feminization of the brain during puberty; and 3) hormonally modulated, sex-specific addition of new neurons and glial cells, as well as loss of neurons, contribute to sexual differentiation of hypothalamic, limbic, and cortical regions during adolescence. This architectural remodeling during the adolescent phase of sexual differentiation of the brain may underlie the known sex differences in vulnerability to addiction and psychiatric disorders that emerge during this developmental period.
    Full-text · Article · Jul 2013 · Hormones and Behavior
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    ABSTRACT: Research suggests that prenatal testosterone exposure may masculinize (i.e., lower) disordered eating (DE) attitudes and behaviors and influence the lower prevalence of eating disorders in males versus females. How or when these effects become prominent remains unknown, although puberty may be a critical developmental period. In animals, the masculinizing effects of early testosterone exposure become expressed during puberty when gonadal hormones activate sex-typical behaviors, including eating behaviors. This study examined whether the masculinizing effects of prenatal testosterone exposure on DE attitudes emerge during puberty in 394 twins from opposite-sex and same-sex pairs. Twin type (opposite sex vs. same sex) was used as a proxy for level of prenatal testosterone exposure because females from opposite-sex twin pairs are thought to be exposed to testosterone in utero from their male co-twin. Consistent with animal data, there were no differences in levels of DE attitudes between opposite-sex and same-sex twins during pre-early puberty. However, during mid-late puberty, females from opposite-sex twin pairs (i.e., females with a male co-twin) exhibited more masculinized (i.e., lower) DE attitudes than females from same-sex twin pairs (i.e., females with a female co-twin), independent of several "third variables" (e.g., body mass index [BMI], anxiety). Findings suggest that prenatal testosterone exposure may decrease DE attitudes and at least partially underlie sex differences in risk for DE attitudes after mid-puberty. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
    No preview · Article · May 2013 · Journal of Abnormal Psychology

Publication Stats

3k Citations
437.49 Total Impact Points


  • 1987-2015
    • Michigan State University
      • • Department of Psychology
      • • Department of Neuroscience
      Ист-Лансинг, Michigan, United States
  • 2014
    • Virginia Commonwealth University
      • Department of Psychiatry
      Ричмонд, Virginia, United States
  • 1999
    • State of Michigan
      Lansing, Michigan, United States
  • 1983-1987
    • Northwestern University
      • Department of Neurobiology
      Evanston, Illinois, United States
  • 1986
    • University of Texas at Austin
      Austin, Texas, United States