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(1 - 11 of 11)
- Title
- Mechanisms mediating life history traits in the spotted hyena (Crocuta crocuta
- Creator
- Lewin, Nora Shannon
- Date
- 2017
- Collection
- Electronic Theses & Dissertations
- Description
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My dissertation focuses on understanding the mechanisms underpinning growth, reproduction, and survival in the spotted hyena. Following a general introductory chapter, my dissertation is composed of four independent research chapters. I begin with Chapter 2 in which my colleagues and I document a positive linear relationship between social dominance rank and telomere length. We also report significant variability in telomere length of high-ranking females among different social groups,...
Show moreMy dissertation focuses on understanding the mechanisms underpinning growth, reproduction, and survival in the spotted hyena. Following a general introductory chapter, my dissertation is composed of four independent research chapters. I begin with Chapter 2 in which my colleagues and I document a positive linear relationship between social dominance rank and telomere length. We also report significant variability in telomere length of high-ranking females among different social groups, suggesting that both social dominance rank and group membership influence this important biomarker of aging. In Chapter 3, we describe the role of juvenile concentrations of the hormone, insulin-like growth-factor -1 (IGF-1), in predicting trade-offs between early-life growth and later-life reproduction and survival among female hyenas. In Chapter 4, I explore IGF-1 as a potential mechanism of female-biased sexual size dimorphism by documenting sex-biased concentrations, sensitivities, and adaptive values of IGF-1 during the early postnatal period. Finally, in Chapter 5, I describe that age-related improvement and senescence in reproductive performance varies with social dominance rank among female hyenas. Cumulatively, my dissertation is an exploration of how physiological mechanisms may be used to understand social, physiological, and evolutionary forces operating in a free-living social carnivore. My work offers a unique contribution to the field of life-history evolution and furthers our understanding of the mechanisms that give rise to it.
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- Title
- Pubertal cytogenesis in neural circuits mediating sex-specific social behaviors
- Creator
- Kim, Jenny Lily
- Date
- 2017
- Collection
- Electronic Theses & Dissertations
- Description
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During puberty and adolescence, the brain experiences significant structural changes that mediate the maturation of sex-specific sociosexual behaviors, such as sexual behavior and intermale aggression. These sex-specific sociosexual behaviors are regulated by sexually dimorphic brain regions such as the posterodorsal medial amygdala (MePD) and ventromedial hypothalamus (VMH). The MePD in laboratory rodents is larger in males than females and is responsible for processing chemosensory signals...
Show moreDuring puberty and adolescence, the brain experiences significant structural changes that mediate the maturation of sex-specific sociosexual behaviors, such as sexual behavior and intermale aggression. These sex-specific sociosexual behaviors are regulated by sexually dimorphic brain regions such as the posterodorsal medial amygdala (MePD) and ventromedial hypothalamus (VMH). The MePD in laboratory rodents is larger in males than females and is responsible for processing chemosensory signals to initiate context-appropriate social behaviors. The VMH is also larger in males than females in rodent species, which is primarily driven by sex differences in the ventrolateral subdivision (VMHvl). The VMHvl is involved in gating male sexual behavior and intermale aggression. Many of these sociosexual behaviors do not emerge until the onset of puberty, suggesting that morphological changes in the MePD and VMHvl during puberty may facilitate their development. Recent studies have discovered that new cells are added to the hypothalamus and amygdala during puberty and a subset of pubertally born cells in the MePD is activated in response to a social encounter. The current dissertation sets out to expand on these findings and examine pubertal cytogenesis in the MePD and VMH using the mouse model. In Chapter 1A, a sex difference in the number of pubertally born cells was revealed in the adult MePD, with males having more pubertally born cells than females. This increase in pubertally born cells in males was dependent on the presence of functional androgen receptors (ARs) and pubertal and adult testosterone. In Chapter 1B, while I initially discovered a sex difference in pubertally born cells in the VMHvl, this finding was not replicated in subsequent studies. In addition, no sex differences were observed in the number of pubertally born cells in sexually monomorphic brain regions (i.e. dorsomedial and central subdivision of the VMH (VMHdm and VMHc, respectively) and dentate gyrus (DG)). These results suggest that the number of pubertally born cells in the adult VMH and DG may not be affected by gonadal hormones. In Chapter 2, I discovered that pubertal, but not adult, ARs promote the increase in pubertally born neurons, but not astrocytes, in the adult male MePD. However, pubertal and adult ARs did not influence the number of pubertally born neurons or astrocytes in the VMH or DG. In Chapter 3, I found that social interaction activated pubertally born cells in the adult male MePD, while social interaction with a male conspecific activated pubertally born cells in the adult male VMHvl and VMHdm. Social interaction did not activate pubertally born cells in the VMHc and DG. These studies demonstrate that gonadal hormones play an important role in regulating the proliferation and/or survival of pubertally born cells in the adult MePD, but not VMH or DG. Furthermore, I provide evidence that pubertally born cells in the MePD, VMHvl, and VMHdm are functionally incorporated into adult neural circuits. Thus, the addition and functional integration of pubertally born cells into neural circuits known to regulate social behavior may be a mechanism by which adult sociosexual behaviors emerge during puberty.
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- Title
- Androgen and serotonin concentrations in spotted hyenas (Crocuta crocuta : physiological predictors and relationships with the social environment
- Creator
- Jones, Sarah Christine
- Date
- 2019
- Collection
- Electronic Theses & Dissertations
- Description
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Animals display a wide range of social behaviors, including social behaviors such as aggression, mating, and parental care. An individual's ability to express the 'right' behavior in the appropriate context is vital to its success. For instance, individuals should engage in mating behavior during the appropriate life history stage (i.e. age, season) and avoid it in inappropriate contexts, such as in the presence of a predator. Neuroendocrine systems are key in allowing individuals to match...
Show moreAnimals display a wide range of social behaviors, including social behaviors such as aggression, mating, and parental care. An individual's ability to express the 'right' behavior in the appropriate context is vital to its success. For instance, individuals should engage in mating behavior during the appropriate life history stage (i.e. age, season) and avoid it in inappropriate contexts, such as in the presence of a predator. Neuroendocrine systems are key in allowing individuals to match their behavior to their current situation, as these systems affect behavior and are also responsive to changes in the environment and in an organism's internal state.Serotonin, a neuromodulator, and androgenic sex steroid hormones are key regulators of aggression and appear to play a central role in matching an organism's aggressive behavior to its social environment. For instance, in many social species living in dominance hierarchies, an individual's social status affects concentrations of serotonin and androgens. Serotonin is a known inhibitor of aggression, whereas androgens often facilitate the expression of aggression; accordingly, social dominance is often negatively correlated with serotonin concentrations and positively correlated with androgens. Still, these patterns are not universal, varying with sex, species, life history stage, and social context.Here, I examined the physiological, demographic, and environmental correlates of serotonin and androgens in a despotic, female-dominant species-the spotted hyena. Specifically, I focused on the relationship between social rank and serotonin/androgens, and its modulators. I first examined predictors of two androgens, testosterone (T) and androstenedione (A4), in pregnant female hyenas. I found a positive relationship between both androgens and social rank. However, this relationship was specific to pregnant females who had previously given birth (multiparous), apparently due to an increase in maternal androgens in high-ranking but not low-ranking females after the birth of their first litter.I then examined the relationship between T and social status in adult females across different reproductive states and social contexts, I found a positive correlation between T and social status in lactating and pregnant females, but not in nulliparous females; again, this pattern appeared to be driven by an increase in high-ranking female T concentrations associated with their first breeding experience. In a comparison of T concentrations in lactating females during periods of relative social stability and instability, I found that T concentrations in low- but not high- ranking females increased during periods of social instability, resulting in the disappearance of the usual positive correlation between social rank and T.Finally, I examined predictors of serotonin concentrations in both male and female hyenas across ontogeny. Serotonin was negatively correlated with social rank in female but not male spotted hyenas. Furthermore, social status at birth was particularly predictive of serotonin, as opposed to social status at the time of physiological sampling, indicating early life social environment may have lifelong effects on serotonergic function.Overall, I found that social status was an important predictor of androgen and serotonin concentrations, but that this relationship was dependent upon characteristics of the individual (e.g. sex, life history stage) and their social environment.
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- Title
- The role of trpc2 in sex-specific brain circuits and behavior
- Creator
- Pfau, Daniel
- Date
- 2019
- Collection
- Electronic Theses & Dissertations
- Description
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The transient receptor potential cation channel 2 (TRPC2) is canonically known for carrying pheromonal information from the vomeronasal organ (VNO) to the brain in rodents. Mice with a disabled TRPC2 gene display drastic changes in sex-specific behaviors, including sexual and aggressive behavior. Specifically, male-male and maternal aggression is absent while both males and females show male-typical mounting behavior directed towards both sexes in a non-preferential manner. In short, sexual...
Show moreThe transient receptor potential cation channel 2 (TRPC2) is canonically known for carrying pheromonal information from the vomeronasal organ (VNO) to the brain in rodents. Mice with a disabled TRPC2 gene display drastic changes in sex-specific behaviors, including sexual and aggressive behavior. Specifically, male-male and maternal aggression is absent while both males and females show male-typical mounting behavior directed towards both sexes in a non-preferential manner. In short, sexual preference seems to be severely disrupted. Several groups have shown that the VNO of TRPC2 knockout (KO) mice show a markedly reduced activation of the VNO in response to pheromones, suggesting that pheromonal signaling via TRPP2 channels in the VNO shape these sex-specific behaviors. However, TRPC2 is also expressed in other tissues, including the reproductive organs, raising the possibility that disruption of TRPC2 function outside the VNO also contributes to changes in adult sex-specific behavior. My dissertation research aims to understand the underpinnings of this behavioral change, examining how the loss of TRPC2 function influences pre- and postnatal development, reproductive success and morphological sex differences in the brain. First, I found that mice lacking TRPC2 display defects in their development, with effects on pubertal timing and pup survival, along with effects on reproductive success. While maternal experience rescued pup survival in TRPC2 KO mice, it did not improve reproductive outcomes. Next, I examined two brain regions implicated in the control of mounting and aggression, the posterodorsal aspect of the medial amygdala and ventromedial hypothalamus. Ux phystilizing a Nissl stain and glial fibrillary acidic protein immunohistochemistry, I determined that TRPC2 KO mice show altered patterns of sex differences at the cellular level in both these regions, offering insight into the neural mechanisms underlying impaired sexual and aggressive behavior. Finally, I examined whether sexual experience can reverse deficits in behavior and rescue the brain's response to pheromones. I found that prolonged sexual experience did not reinstate normal sexual preference nor recover the brain response to pheromones. These experiments suggest TRPC2 function, driven by pheromones and possibly other incoming signals, participates in organizing sex-specific behavior and brain circuitry. TRPC2 function outside the VNO may also impact adult sex-specific behaviors.
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- Title
- Peripartum plasticity in the serotonergic dorsal raphe : implications for postpartum socioemotional behavior and physiology
- Creator
- Holschbach, Mary A.
- Date
- 2015
- Collection
- Electronic Theses & Dissertations
- Description
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Postpartum rats are highly maternal and show high aggression and low anxiety compared to nulliparous rats. To promote these dramatic changes in behavior, new mothers experience equally dramatic endocrine changes that elicit widespread neural plasticity. This neural plasticity includes cell birth and death in several regions of the peripartum forebrain, but such plasticity has never been reported in the dorsal raphe (DR), a midbrain site that provides most of the forebrain’s serotonin. Because...
Show morePostpartum rats are highly maternal and show high aggression and low anxiety compared to nulliparous rats. To promote these dramatic changes in behavior, new mothers experience equally dramatic endocrine changes that elicit widespread neural plasticity. This neural plasticity includes cell birth and death in several regions of the peripartum forebrain, but such plasticity has never been reported in the dorsal raphe (DR), a midbrain site that provides most of the forebrain’s serotonin. Because 1) postpartum lesions of the dorsal raphe reduce offspring development and survival, 2) serotonin affects postpartum social behaviors including caregiving and aggression, and 3) serotonin modulates anxiety in nulliparous males and females, I hypothesized that motherhood alters DR plasticity and serotonin synthesis/metabolism to support postpartum changes in socioemotional behaviors. To test this hypothesis, I examined effects of reproductive state and maternal experience on DR cell proliferation, newborn cell survival, cell death, and many aspects of the serotonin synthesis/metabolism pathway, then tested postpartum social and emotional behavior after lesioning the serotonergic DR. I discovered that although an equal number of cells are born in the DR of virgin, pregnant, and postpartum rats, fewer cells survived into the late postpartum period compared to cells surviving into the early postpartum period. These late postpartum females also had the highest levels of cell death within the DR. Next, I determined that interacting with the litter reduced cell survival and increased cell death in the DR of late postpartum rats. These effects were not due to high maternal corticosterone because adrenalectomized and sham-operated postpartum rats had equivalent DR cell survival. DR newborn cell survival and cell death were related to changes in serotonin synthesis and metabolism because late postpartum rats also had lower levels of serotonin’s precursor (5-HTP) and metabolite (5-HIAA) than early postpartum rats. To begin to test the functional significance of these changes in neuroplasticity and neurochemical function, I performed serotonin-specific DR lesions using a saporin-conjugated toxin targeting the serotonin transporter. Lesioning the DR altered numerous postpartum behaviors. During undisturbed observations, lesioned animals actively nursed pups (in kyphosis) more and licked pups less. Lesioning the DR did not greatly affect anxiety-like behavior, but did reduce maternal aggression. These data demonstrate that the DR is a site of significant peripartum plasticity, and that, along with this plasticity, there are concurrent changes in local serotonin synthesis and metabolism. These neurochemical changes may guide postpartum behavioral adaptations because lesioning the DR of new mothers had numerous effects on postpartum social behaviors. Taken together, these data suggest that the DR is an integral part of the maternal neural network that guides the initiation, modulation, and regression of postpartum behaviors.
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- Title
- Androgen toxicity on neuromuscular physiology in a novel model of SBMA
- Creator
- Oki, Kentaro
- Date
- 2013
- Collection
- Electronic Theses & Dissertations
- Description
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Spinal bulbar muscular atrophy (SBMA) is a progressive motor disease that appears only in men around mid-life and results in limb weakness, dysphagia (swallowing difficulties), and dysarthria (speech difficulties). The disease is believed to be neurogenic, originating from motoneuron dysfunction and its slow progressive death. Thus, most of the studies characterizing the disease in mice have focused on motoneuron as the site of disease although there is some clinical evidence suggesting...
Show moreSpinal bulbar muscular atrophy (SBMA) is a progressive motor disease that appears only in men around mid-life and results in limb weakness, dysphagia (swallowing difficulties), and dysarthria (speech difficulties). The disease is believed to be neurogenic, originating from motoneuron dysfunction and its slow progressive death. Thus, most of the studies characterizing the disease in mice have focused on motoneuron as the site of disease although there is some clinical evidence suggesting skeletal muscle may be an important site of disease. SBMA is caused by a mutation that leads to an expansion of CAG repeats coding for glutamine in the androgen receptor (AR) gene, and the male-specific phenotype is believed to be androgen-dependent as females carrying the mutation have little to no symptoms. The male-specific disease phenotype has been replicated in mouse models expressing similar mutations and can be improved with castration, reinforcing that the disease is androgen-dependent. Furthermore, female mice in these models are asymptomatic and only exhibit disease symptoms with androgen treatment. Although a CAG expansion in the AR gene is thought to underlie the disease, a similar phenotype is observed in a transgenic (Tg) mouse line engineered to express a rat AR cDNA with a wild type (WT) number of glutamine residues (22) at very high levels exclusively in skeletal muscle fibers. Although alteration of gene and protein expression is exclusive to the skeletal muscles, mice from this myogenic (141) model exhibit a phenotype similar to the other CAG-expanded mouse models of SBMA. Tg 141 female mice that exhibit an androgen-dependent loss of motor function after 3-5 days of testosterone (T) treatment exhibit skeletal muscle dysfunction, recorded by electrically stimulating isolated preparations of the extensor digitorum longus (EDL) and the soleus (SOL), prototypical fast- and slow-twitch muscles, respectively. T treatment in female 141 Tg mice over 3-5 days was enough to induce a precipitous decrease in force production in both muscles and alterations to kinetics during contractions in the EDL. To confirm that skeletal muscles could be a primary site of disease during SBMA, male mice of the same 141 model, as well as two other SBMA mouse models were examined. The other models were one expressing the full-length human AR with 97 CAG repeats (97Q model) and another expressing 113 CAG repeats in the first exon of the AR gene. Muscle dysfunction in the other models would further support myogenic contributions as being critical to the SBMA motor phenotype. Motor dysfunction was recorded in all mouse models, and male mice from the 141 and 97Q models exhibited dysfunction in the EDL and SOL. All muscles exhibited some deficit during force production, and contraction kinetics were altered in the EDL of Tg 141 males. These results indicate that severe muscle dysfunction can underlie the phenotype during SBMA, and androgens can act on the skeletal muscles to induce motor weakness. Furthermore, skeletal muscles may be an important target for therapeutics that could ameliorate disease symptoms.
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- Title
- Traumatic stress responses in rats reveal fundamental sex differences that mirror PTSD in men and women
- Creator
- Pooley, Apryl E., 1986-
- Date
- 2017
- Collection
- Electronic Theses & Dissertations
- Description
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Post-traumatic stress disorder (PTSD) develops after exposure to trauma and is associated with dysfunction in the normal stress response. Women are twice as likely as men to develop PTSD and tend to experience different symptoms and comorbidities than men, but the neurobiological basis for these pervasive sex differences is poorly understood due to the overwhelming male bias in the preclinical research. My dissertation work tested the novel hypothesis that the neurobiological mechanisms...
Show morePost-traumatic stress disorder (PTSD) develops after exposure to trauma and is associated with dysfunction in the normal stress response. Women are twice as likely as men to develop PTSD and tend to experience different symptoms and comorbidities than men, but the neurobiological basis for these pervasive sex differences is poorly understood due to the overwhelming male bias in the preclinical research. My dissertation work tested the novel hypothesis that the neurobiological mechanisms underlying the traumatic stress response in male and female rats are fundamentally different and may be related to normal sex differences in circulating levels of adult gonadal hormones. These experiments are the first to compare adult male and female rats across two rodent models of PTSD, single prolonged stress and predator exposure. I report a highly sex-specific traumatic stress response that recapitulates fundamental differences of PTSD in men and women. Surprisingly, these sex differences were largely independent of adult circulating gonadal hormones, housing conditions, and types of stress. Two standard measures, the acoustic startle response and dexamethasone suppression test to measure the negative feedback control of the stress hormone response, suggest that female rats, unlike male rats, are resilient to the effects of traumatic stress. However, other measures like sucrose preference and social interaction make it clear that females are not resilient, but simply respond differently to trauma than males. Dramatic sex differences in how trauma affects cFos activation and glucocorticoid receptor expression in the brain lend further support to the idea that the trauma response of males and females is fundamentally different, and likely determined prior to adulthood. Factors that mediate differences in how individuals adjust after trauma are attractive targets for the prevention and treatment of PTSD, and identifying such factors of resilience depends on understanding the various ways the traumatic stress response manifests in different individuals. I propose that sex differences offer a promising inroad for addressing this issue.
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- Title
- The neuroprotective potential of STN DBS and the role of BDNF
- Creator
- Fischer, David Luke
- Date
- 2015
- Collection
- Electronic Theses & Dissertations
- Description
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Parkinson’s disease (PD) is a chronic, neurodegenerative disease that affects one percent of the population over the age of sixty. To our knowledge, there is no therapy that can slow the progression of the disease. Deep brain stimulation (DBS) of either the subthalamic nucleus (STN) or the globus pallidus interna (GPi) is well established to provide significant therapeutic efficacy in alleviating the motor symptoms of PD, yet our understanding of effects on disease progression remains limited...
Show moreParkinson’s disease (PD) is a chronic, neurodegenerative disease that affects one percent of the population over the age of sixty. To our knowledge, there is no therapy that can slow the progression of the disease. Deep brain stimulation (DBS) of either the subthalamic nucleus (STN) or the globus pallidus interna (GPi) is well established to provide significant therapeutic efficacy in alleviating the motor symptoms of PD, yet our understanding of effects on disease progression remains limited. Previous studies have shown that long-term, high-frequency stimulation of the STN halts degeneration of the substantia nigra induced by intrastriatal 6-hydroxydopamine (6-OHDA) injections and significantly increases brain-derived neurotrophic factor (BDNF) in the nigrostriatal system, primary motor cortex and entopeduncular nucleus (EP). These results suggest that STN DBS can induce plasticity within basal ganglia circuitry and has the potential to provide neuroprotection in PD.In order to examine the role of BDNF in the neuroprotective effects of STN DBS, I examined in our 6-OHDA rat model if blockade of the trophic receptor for BDNF, tropomyosin-related kinase type 2 (trkB), would alter the afforded protection. I also examined the effect of trkB antagonism on the recovery of motor function provided by STN DBS for unilaterally lesioned rats. Beyond elucidation of the mechanism for STN DBS-mediated neuroprotection, I evaluated if STN DBS would similarly facilitate nigral neuroprotection against α-synuclein overexpression-mediated toxicity. Lastly, I evaluated if DBS of the EP, the homologous structure of the GPi in the rat, would result in similar results as STN stimulation, namely alleviation of a unilateral motor deficit, nigral neuroprotection and increased BDNF. The data demonstrate that BDNF plays a critical role in the neuroprotective effects of STN DBS and in the alleviation of a unilateral motor deficit. The data also show that STN DBS is unable to provide neuroprotection against α-synuclein overexpression-mediated insult, but I call into question the usefulness of this model for the question of if STN DBS is disease modifying. I also present data that support abandoning EP DBS in the rat as an appropriate model of GPi DBS for PD. I conclude with remarks on the implications of this work for the clinic, including the use of a common variant in the gene for BDNF as a biomarker that may allow the development of ‘precision medicine’ approaches for the refinement of current medical practice guidelines for PD.
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- Title
- Prenatal testosterone exposure and developmental differences in risk for disordered eating
- Creator
- Culbert, Kristen Marie
- Date
- 2011
- Collection
- Electronic Theses & Dissertations
- Description
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Prenatal testosterone may masculinize (i.e., lower) risk for disordered eating and account for sex differences in prevalence, yet how these effects emerge and whether these effects remain static across development is unknown. Opposite-sex (OS) twins provide a natural design to investigate such effects, as OS female twins are thought to be exposed to elevated testosterone in utero from their male co-twin. Although OS female twins have shown masculinized disordered eating relative to other...
Show morePrenatal testosterone may masculinize (i.e., lower) risk for disordered eating and account for sex differences in prevalence, yet how these effects emerge and whether these effects remain static across development is unknown. Opposite-sex (OS) twins provide a natural design to investigate such effects, as OS female twins are thought to be exposed to elevated testosterone in utero from their male co-twin. Although OS female twins have shown masculinized disordered eating relative to other females, findings have been mixed. The current research used a series of studies to investigate whether there are developmental differences in the masculinizing/protective effects of prenatal testosterone exposure in risk for disordered eating. Study 1 examined whether age moderates the masculinizing effects of prenatal testosterone on disordered eating. OS female twins have shown masculinized disordered eating in early young adulthood, but these effects have not been robustly observed in other time periods, e.g., mid-to-late adolescence or mid-to-late young adulthood. Participants included 764 male and female twins (ages 15-30) and 74 non-twin females (ages 15-23) from the Michigan State University Twin Registry (MSUTR). Two well-validated measures (i.e., Minnesota Eating Behaviors Survey and the Eating Disorder Examination Questionnaire) were used to assess several disordered eating symptoms. Results indicated no evidence for masculinization of disordered eating in OS female twins during mid-to-late adolescence (ages 15-20). In contrast, OS female twins showed substantially masculinized levels of disordered eating across several scales in early young adulthood (ages 21-23). Masculinization of disordered eating in OS female twins also appeared to be present in mid-to-late young adulthood (ages 24-30), but effects were weaker and more variable across disordered eating scales. These findings suggest developmental windows of expression for the protective effects of prenatal testosterone on disordered eating, with effects strongest under "average" risk periods (i.e., young adulthood) and attenuated under higher risk periods (i.e., mid-to-late adolescence, the peak period for eating disorder onset). Study 2 was a translational extension of study 1 that aimed to determine if prenatal testosterone's masculinizing effects on disordered eating only become prominent during young adulthood (as observed in study 1), or whether, as predicted by animal data, masculinization effects emerge with puberty. In female animals, early testosterone exposure decreases sensitivity to ovarian hormones during and after puberty. Thus, one potential mechanism for prenatal testosterone's effects on disordered eating may be via decreased sensitivity to the activating effects of ovarian hormones on disordered eating risk. Study 2 examined whether puberty underlies the emergence of prenatal testosterone's masculinization of disordered eating, independent of the confounding effects of several other factors (e.g., adiposity, mood, autonomy, being reared with a brother). Participants included 394 male and female twins and 63 non-twin females (ages 10-15) from the MSUTR. Well-validated measures assessed disordered eating, pubertal status, mood symptoms, and autonomy difficulties. Body mass index was used as a marker of adiposity. Disordered eating did not differ amongst twin types in pre-early puberty, whereas OS female twins fell intermediate to males and SS female twins on levels of disordered eating during mid-late puberty. Masculinization effects in mid-late pubertal OS female twins were not accounted for by adiposity, mood symptoms, autonomy difficulties or being reared with a brother. Taken together, findings indicate that other key factors (e.g., sensitivity to circulating gonadal hormones) likely underlie prenatal testosterone's protective effects on disordered eating.
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- Title
- The effects of target sex, presence of others, and attractiveness on desire for targets : a re-examination of Hill and Buss (2008)
- Creator
- Shaw, Allison Zorzie
- Date
- 2012
- Collection
- Electronic Theses & Dissertations
- Description
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Research on sexual selection has argued that males' and females' mate choice strategies differ due to different biological reproductive pressures demanded of each. Hill and Buss (2008) argue that due to these differing pressures and the subsequent difference in mate choice strategies used by males and females, the two sexes additionally differ in their use of social information when deciding upon a mate. Hill and Buss (2008) propose that when a male target is in the presence of opposite sex...
Show moreResearch on sexual selection has argued that males' and females' mate choice strategies differ due to different biological reproductive pressures demanded of each. Hill and Buss (2008) argue that due to these differing pressures and the subsequent difference in mate choice strategies used by males and females, the two sexes additionally differ in their use of social information when deciding upon a mate. Hill and Buss (2008) propose that when a male target is in the presence of opposite sex others, female subjects will desire him more than if the same male target were presented with same sex others or alone (desirability enhancing effect); alternatively, a female target presented with opposite sex others is desired more by male subjects than the same female target presented with same sex others or alone (desirability diminishing effect). Additionally, Hill and Buss (2008) provide testable reasons for why the desirability effects exert a sex difference, but do not actually test such propositions. The present paper utilized a 2 X 2 X 3 (target sex, attractiveness, presence of others) design in order to replicate Hill & Buss' (2008) findings. Furthermore, the present paper proposed an alternative explanation for their findings (attractiveness effect) and examined this proposed alternative explanation. Finally, the present paper developed testable models derived from the desirability and attractiveness effects. The pattern of means obtained in this study is inconsistent with Hill and Buss' (2008) previous findings and the models derived from their work. The data were also inconsistent with the hypothesized attractiveness effect and model, however, upon closer examination a post-hoc revised attractiveness model was proposed, and the data were consistent with it. Finally, this paper argues for a reconceptualization of desirability and mate choice.
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- Title
- Pathology at the neuromuscular junction in mouse models of spinal bulbar muscular atrophy
- Creator
- Poort, Jessica Erin
- Date
- 2014
- Collection
- Electronic Theses & Dissertations
- Description
-
Spinal bulbar muscular atrophy (SBMA) is a progressive, late onset neuromuscular disease that results in muscle weakness and atrophy, as well as motoneuron death in men. While pathology at the neuromuscular junction (NMJ) is noted in numerous neurodegenerative diseases, disease-related changes at the NMJ in SBMA have not been explored. Characterizing such changes is not only important for determining whether the NMJ has any role in the functional changes underlying motor dysfunction, but also...
Show moreSpinal bulbar muscular atrophy (SBMA) is a progressive, late onset neuromuscular disease that results in muscle weakness and atrophy, as well as motoneuron death in men. While pathology at the neuromuscular junction (NMJ) is noted in numerous neurodegenerative diseases, disease-related changes at the NMJ in SBMA have not been explored. Characterizing such changes is not only important for determining whether the NMJ has any role in the functional changes underlying motor dysfunction, but also in determining how such potential pathology at the NMJ develops as disease progresses. If for example, pathology emerges first at the NMJ followed by motoneuron death, then the NMJ offers future promise as a therapeutic target for preventing or reversing symptoms of SBMA before motoneurons are lost. We evaluated three different mouse models of SBMA, one overexpressing a wildtype androgen receptor (AR) exclusively in muscle fibers (so called "myogenic" model), a second which expressed the endogenous AR gene with the first exon of the human mutant AR gene "knocked in" (the so called "knock-in" model), and a final model that broadly expresses a full length human AR transgene harboring the SBMA mutation (the so called "97Q" model). Using both confocal microscopy and electron microscopy, I found that all three mouse models show a pathological fragmentation of the NMJ suggestive of functionally weakened synapses. Other changes at the neuromuscular synapse suggesting decreases in synaptic strength that were found in some but not all models include a decline in the number of docked vesicles ready for release in nerve terminals, a widening of synaptic clefts, simplified postsynaptic folds, and an abnormal accumulation of synaptic vesicle and neurofilament proteins. Retrograde axonal transport of endosomes was also characterized in the 97Q model using live imaging confocal microscopy. Despite previously published data, I found no evidence for a disease-related defect in retrograde transport in the 97Q model. The strikingly abnormal morphology of NMJs in all three models raises the possibility that synaptic function is impaired. Such synaptic dysfunction may contribute to or underlie the impairments in motor function associated with SBMA.
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