Joanne Weinberg

Child & Family Research Institute, Vancouver, British Columbia, Canada

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Publications (152)516.51 Total impact

  • W. Comeau · K. Lee · J. Weinberg

    No preview · Article · Dec 2015

  • No preview · Article · Dec 2015
  • Ni Lan · Kim G C Hellemans · Linda Ellis · Joanne Weinberg
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    ABSTRACT: Background: Prenatal alcohol exposure (PAE) results in dysregulation of the offspring hypothalamic-pituitary-adrenal (HPA) axis, increasing sensitivity to stressors and vulnerability to stress-related disorders. We have previously shown that exposure to chronic mild stress (CMS) in adulthood significantly increases anxiety-like behaviors (elevated plus maze) in PAE males and females compared to controls. To explore neurobiological mechanisms linking HPA dysregulation and altered anxiety-like behavior, we investigated neuropeptide (corticotropin-releasing hormone [CRH] and arginine vasopressin [AVP]) expression in brain areas involved in the stress neurocircuitry of animals from this previous behavioral study. Methods: Adult PAE, pair-fed (PF), and ad libitum fed control (C) male and female offspring exposed to CMS or remaining undisturbed (non-CMS) were terminated 30 minutes following behavioral testing. Results: In the paraventricular nucleus, CMS increased CRH mRNA levels in PAE compared to PF and C males and increased AVP mRNA levels in PAE compared to C males, with no differential effects for CRH or AVP in females. In the central nucleus of the amygdala, there was an increase in CRH mRNA expression overall, regardless of CMS condition or sex, in PAE compared to C animals. Moreover, in PF males, CMS increased AVP mRNA levels in the paraventricular nucleus, resulting in a decreased CRH/AVP ratio compared to PAE males, and decreased amygdala CRH mRNA compared to that in the non-CMS condition. Conclusions: CMS differentially altered central HPA peptide expression in PAE and PF animals compared to their control counterparts, with a possible shift toward greater CRH mediation of HPA regulation in PAE males, and greater AVP mediation of HPA regulation in PF males. However, changes in CRH and AVP expression do not align fully with the anxiogenic profile observed in our previous behavior study, suggesting that other neuronal substrates and limbic forebrain regions also contribute to increased anxiety-like behavior following CMS.
    No preview · Article · Nov 2015 · Alcoholism Clinical and Experimental Research
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    ABSTRACT: Sprague Dawley rats from different vendor colonies display divergent responses in a variety of experimental paradigms. An adjuvant-induced arthritis (AA) model of human rheumatoid arthritis was used to examine immune and endocrine responses to inflammatory challenge in Sprague Daley rats from Charles River and Harlan colonies. Rats were injected with either complete Freund's adjuvant (CFA) or physiological saline (control), weights and paw volumes measured over 15 days, and blood and tissue collected on day 16 post-injection. Overall, Harlan rats developed more severe AA than Charles River rats. In addition, despite comparable corticosterone levels, corticosteroid binding globulin (CBG) levels were lower in Harlan compared to Charles River rats in the absence of inflammation, suggesting that a lower corticosterone reservoir in Harlan rats may underlie their greater susceptibility to inflammation. With increasing AA severity, there was an increase in plasma corticosterone (total and free) and a decrease in CBG in Charles River and Harlan rats. Finally, contrasting patterns of cytokine activation were observed in the hind paw suggesting a reliance on different cytokine networks at different stages of inflammation, with Charles River rats exhibiting increased TNF-α, MCP-1, KC/GRO and IL-1β in the absence of clinical signs of arthritis, whereas Harlan had increased TNF- α, MCP-1 and IL-6 with mild-moderate arthritis. These colony-specific differences in endocrine and immune responses to AA in Sprague Dawley rats must be considered when comparing data from different laboratories and could be exploited to provide insight into physiological changes and therapeutic outcomes in arthritis and other inflammatory disorders.
    No preview · Article · Sep 2015 · Endocrinology
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    ABSTRACT: This chapter reviews the development and use of animal models in research on Fetal Alcohol Spectrum Disorder, highlighting methodological issues. The development of suitable animal models in this field has been crucial in investigating the wide range of effects of prenatal alcohol exposure under tightly controlled conditions, as well as factors that can influence the severity of effects observed, and the mechanisms mediating those effects. Animal models in this field have been critical in demonstrating that alcohol is a powerful teratogen with serious neurodevelopmental consequences, a fact that was met with skepticism by many in the scientific community when Fetal Alcohol Syndrome was first described. The review begins with a discussion of the various animal models in the field, highlighting the benefits and limitations of each model. Although it is not inclusive, this chapter aims to provide an overview of the challenges that FASD researchers have had in developing animal models that have construct, face and etiological validity. We then discuss the factors that must be addressed in the development of an animal model, including dose and timing of alcohol exposure, blood alcohol levels (BALs), mode of alcohol administration, nutritional considerations, maternal-pup interactions, housing considerations, and strain differences. The chapter then moves on to discuss in some detail the model of chronic, moderate prenatal alcohol exposure utilized in our research with Sprague-Dawley rats. A detailed discussion of our breeding, feeding, culling, and weaning procedures is provided, including the specifics of our liquid diets and feeding schedule, with particular consideration of the issue of pair-feeding. Finally, detailed notes are provided to explain the rationale underlying methodology and procedures described in our protocol.
    No preview · Article · Sep 2015 · Neuromethods
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    ABSTRACT: Child executive functions (cognitive flexibility, inhibitory control, working memory) are key to success in school. Cortisol, the primary stress hormone, is known to affect cognition; however, there is limited information about how child cortisol levels, parenting factors and child care context relate to executive functions in young children. The aim of this study was to examine relationships between child cortisol, parenting stress, parent coping, and daycare quality in relation to executive functions in children aged 3-5 years. We hypothesized that (1) poorer executive functioning would be related to higher child cortisol and higher parenting stress, and (2) positive daycare quality and positive parent coping style would buffer the effects of child cortisol and parenting stress on executive functions. A total of 101 children (53 girls, 48 boys, mean age 4.24 years ±0.74) with complete data on all measures were included. Three saliva samples to measure cortisol were collected at the child's daycare/preschool in one morning. Parents completed the Behavior Rating Inventory of Executive Function - Preschool Version (BRIEF-P), Parenting Stress Index (PSI), and Ways of Coping Questionnaire (WCQ). The Early Childhood Environment Rating Scale - Revised (ECERS-R) was used to measure the quality of daycare. It was found that children with poorer executive functioning had higher levels of salivary cortisol, and their parents reported higher parenting stress. However, parent coping style and quality of daycare did not modulate these relationships. Identifying ways to promote child executive functioning is an important direction for improving school readiness.
    Full-text · Article · Sep 2015 · Child Neuropsychology
  • N Lan · M.P.Y. Chiu · L Ellis · J Weinberg
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    ABSTRACT: Adverse intrauterine environments increase vulnerability to chronic diseases across the lifespan. The hypothalamic-pituitary-adrenal (HPA) axis, which integrates multiple neuronal signals and ultimately controls the response to stressors, may provide a final common pathway linking early adversity and adult disease. Both prenatal alcohol exposure (PAE) and prenatal stress (PS) induce a hyperresponsive HPA phenotype in adulthood. As glucocorticoids are pivotal for the normal development of many fetal tissues including the brain, we used animal models of PAE and PS to investigate possible mechanisms underlying fetal programming of glucocorticoid signaling in the placenta and fetal brain at gestation day (GD) 21. We found that both PAE and PS dams had higher corticosterone levels than control dams. However, 11β-HSD2 enzyme levels were increased in PAE and unchanged in PS placentae, although there were no differences in 11β-HSD1 levels. Moreover, only PAE fetuses showed decreased body weight and increased placental weight, and hence a lower fetal/placental weight ratio, a marker of placenta efficiency, compared to all other prenatal groups. Importantly, PAE and PS differentially altered corticosteroid receptor levels in placentae and brains. In the PS condition, maternal corticosterone was negatively correlated with both 11β-HSD1 and MR proteins levels in male and female placentae, whereas in the PAE condition, there were trends for a positive correlation between maternal corticosterone and 11β-HSD1, regardless of sex, and a negative correlation between maternal alcohol intake and MR in male placentae. In fetal brains, sexually dimorphic changes in MR and GR levels, and the MR/GR ratio seen in C fetuses were absent in PAE and PS fetuses. In addition, PS but not PAE female fetuses had higher MR and lower GR expression levels in certain limbic areas compared to C female fetuses. Thus the similar adult HPA hyperresponsive phenotype in PAE and PS animals likely occurs through differential effects on glucocorticoid signaling in the placenta and fetal brain. Copyright © 2015. Published by Elsevier Ltd.
    No preview · Article · Sep 2015 · Neuroscience
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    ABSTRACT: Early stress in the form of repetitive neonatal pain, in infants born very preterm, is associated with long-term dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis and with poorer cognitive performance. Brain-derived neurotrophic factor (BDNF) which is important in synaptic plasticity and cognitive functions is reduced by stress. Therefore the BDNF Val66Met variant, which affects secretion of BDNF, may interact with early exposure to pain-related stress in children born very preterm, to differentially affect HPA regulation that in turn may be associated with altered cognitive performance.
    Full-text · Article · Aug 2015 · Neuroscience
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    ABSTRACT: Chronic alcohol consumption negatively affects health, and has additional consequences if consumption occurs during pregnancy as prenatal alcohol exposure adversely affects offspring development. While much is known on the effects of prenatal alcohol exposure in offspring less is known about effects of alcohol in dams. Here, we examine whether chronic alcohol consumption during gestation alters maternal behavior, hippocampal neurogenesis and HPA axis activity in late postpartum female rats compared with nulliparous rats. Rats were assigned to alcohol, pair-fed or ad libitum control treatment groups for 21 days (for pregnant rats, this occurred gestation days 1-21). Maternal behavior was assessed throughout the postpartum period. Twenty-one days after alcohol exposure, we assessed doublecortin (DCX) (an endogenous protein expressed in immature neurons) expression in the dorsal and ventral hippocampus and HPA axis activity. Alcohol consumption during pregnancy reduced nursing and increased self-directed and negative behaviors, but spared licking and grooming behavior. Alcohol consumption increased corticosterone and adrenal mass only in nulliparous females. Surprisingly, alcohol consumption did not alter DCX-expressing cell density. However, postpartum females had fewer DCX-expressing cells (and of these cells more immature proliferating cells but fewer postmitotic cells) than nulliparous females. Collectively, these data suggest that alcohol consumption during pregnancy disrupts maternal care without affecting HPA function or neurogenesis in dams. Conversely, alcohol altered HPA function in nulliparous females only, suggesting that reproductive experience buffers the long-term effects of alcohol on the HPA axis. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Full-text · Article · Jul 2015 · Psychoneuroendocrinology
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    ABSTRACT: Prenatal alcohol exposure (PAE) programs the fetal hypothalamic-pituitary-adrenal (HPA) axis, resulting in HPA dysregulation and hyperresponsiveness to stressors in adulthood. Molecular mechanisms mediating these alterations are not fully understood. Disturbances in one carbon metabolism, a source of methyl donors for epigenetic processes, contributes to alcoholic liver disease. We assessed whether PAE affects one carbon metabolism (including Mtr, Mat2a, Mthfr, and Cbs mRNA) and programming of HPA function genes (Nr3c1, Nr3c2, Slc6a4) in offspring from ethanol-fed (E), pair-fed (PF), and ad libitum-fed control (C) dams. At gestation day 21, plasma total homocysteine and methionine concentrations were higher in E compared to C dams, and E fetuses had higher plasma methionine concentrations and lower whole brain Mtr and Mat2a mRNA compared to C fetuses. In adulthood (55 days), hippocampal Mtr and Cbs mRNA were lower in E compared to C males, whereas Mtr, Mat2a, Mthfr, and Cbs mRNA were higher in E compared to C females. We found lower Nr3c1 mRNA and lower NGFI-A protein in the hippocampus of E compared to PF females, whereas hippocampal Slc6a4 mRNA was higher in E than C males. By contrast, hypothalamic Slc6a4 mRNA lower in E males and females compared to C offspring. This was accompanied by higher hypothalamic Slc6a4 mean promoter methylation in E compared to PF females. These findings demonstrate that PAE is associated with alterations in one carbon metabolism and has long-term and region-specific effects on gene expression in the brain. These findings advance our understanding of HPA dysregulation associated with PAE. Copyright © 2015, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.
    Preview · Article · Jul 2015 · AJP Regulatory Integrative and Comparative Physiology
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    ABSTRACT: We previously identified gene expression changes in the prefrontal cortex and hippocampus of rats prenatally exposed to alcohol under both steady-state and challenge conditions [8]. In this study, adult female rats from three prenatal treatment groups (ad libitum-fed control, pair-fed, and ethanol-fed) were injected with physiological saline solution or complete Freund's adjuvant (CFA) to induce arthritis (adjuvant-induced arthritis, AA). The prefrontal cortex and hippocampus were collected 16 days (peak of arthritis) or 39 days (during recovery) following injection, and whole genome gene expression was assayed using Illumina's RatRef-12 expression microarray. Here, we provide additional metadata, detailed explanations of data pre-processing steps and quality control, as well as a basic framework for the bioinformatic analyses performed. The datasets from this study are publicly available on the GEO repository (accession number GSE63561).
    Full-text · Article · Jun 2015
  • Wendy L Comeau · Kristen Lee · Katie Anderson · Joanne Weinberg
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    ABSTRACT: Abnormal activity of stress hormone (hypothalamic-pituitary-adrenal [HPA]), and gonadal hormone (hypothalamic-pituitary-gonadal [HPG]) systems is reported following prenatal alcohol exposure (PAE). PAE increases vulnerability of brain regions involved in regulation of these systems to stressors or challenges during sensitive periods of development, such as adolescence. In addition, HPA and HPG functions are linked to higher order functions such as executive function (EF), with dysregulation of either system adversely affecting EF processes, including attention and response inhibition, that influence cognition. However, how HPA and HPG systems interact to influence cognitive performance in individuals with an FASD is not fully understood. To investigate, we used a rat model of moderate PAE. Adolescent female PAE and control offspring were exposed to 10days of chronic mild stress (CMS) and cognitive function was assessed on the radial arm maze (RAM) in adulthood. On the final test day, animals were sacrificed, with blood collected for hormone analyses, and vaginal smears taken to assess estrus stage at the time of termination. Analyses showed that adolescent CMS significantly increased levels of CORT and RAM errors during proestrus in adult PAE but not control females. Moreover, CORT levels were correlated with estradiol levels and with RAM errors, but only in PAE females, with outcome dependent on adolescent CMS condition. These results suggest that PAE increases sensitivity to the influences of stress and gonadal hormones on cognition, and thus, in turn, that HPA and HPG dysregulation may underlie some of the deficits in executive function described previously in PAE females. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Feb 2015 · Physiology & Behavior
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    ABSTRACT: Background Prenatal alcohol exposure (PAE) is associated with alterations in numerous physiological systems, including the stress and immune systems. We have previously shown that PAE increases the course and severity of arthritis in an adjuvant-induced arthritis (AA) model. While the molecular mechanisms underlying these effects are not fully known, changes in neural gene expression are emerging as important factors in the etiology of PAE effects. As the prefrontal cortex (PFC) and hippocampus (HPC) play key roles in neuroimmune function, PAE-induced alterations to their transcriptome may underlie abnormal steady-state functions and responses to immune challenge. This study examined brains from adult PAE and control females from our recent AA study to determine whether PAE causes long-term alterations in gene expression and whether these mediate the altered severity and course of arthritis in PAE females.Methods Adult females from PAE, pair-fed (PF), and ad libitum-fed control (C) groups were injected with either saline or complete Freund's adjuvant. Animals were terminated at the peak of inflammation or during resolution (Days 16 and 39 postinjection, respectively); cohorts of saline-injected PAE, PF, and C females were terminated in parallel. Gene expression was analyzed in the PFC and HPC using whole-genome mRNA expression microarrays.ResultsSignificant changes in gene expression in both the PFC and HPC were found in PAE compared to controls in response to ethanol exposure alone (saline-injected females), including genes involved in neurodevelopment, apoptosis, and energy metabolism. Moreover, in response to inflammation (adjuvant-injected females), PAE animals showed unique expression patterns, while failing to exhibit the activation of genes and regulators involved in the immune response observed in control and pair-fed animals.Conclusions These results support the hypothesis that PAE affects neuroimmune function at the level of gene expression, demonstrating long-term effects of PAE on the central nervous system response under steady-state conditions and following an inflammatory insult.
    No preview · Article · Feb 2015 · Alcoholism Clinical and Experimental Research
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    ABSTRACT: Early life stress can alter hypothalamic pituitary adrenal (HPA) axis function. Differences in cortisol levels have been found in preterm infants exposed to substantial procedural stress during neonatal intensive care, compared to infants born full-term, but only a few studies investigated whether altered programming of the HPA axis persists past toddler age. Further, there is a dearth of knowledge of what may contribute to these changes in cortisol. This prospective cohort study examined the cortisol profiles in response to the stress of cognitive assessment, as well as the diurnal rhythm of cortisol, in children (n = 129) born at varying levels of prematurity (24–32 weeks gestation) and at full-term (38–41 weeks gestation), at age 7 years. Further, we investigated the relationships among cortisol levels and neonatal procedural pain-related stress (controlling for multiple medical confounders), concurrent maternal factors (parenting stress, depressive and anxiety symptoms) and children's behavioral problems. For each aim we investigate acute cortisol response profiles to a cognitive challenge as well as diurnal cortisol patterns at home. We hypothesized that children born very preterm will differ in their pattern of cortisol secretion from children born full-term, possibly depended on concurrent child and maternal factors, and that exposure to neonatal pain-related stress would be associated with altered cortisol secretion in children born very preterm, possibly in a sex-dependent way. Saliva samples were collected from 7-year old children three times during a laboratory visit for assessment of cognitive and executive functions (pretest, mid-test, end—study day acute stress profile) and at four times over two consecutive non-school days at home (i.e. morning, mid-morning, afternoon and bedtime—diurnal rhythm profile). We found that cortisol profiles were similar in preterm and full-term children, albeit preterms had slightly higher cortisol at bedtime compared to full-term children. Importantly, in the preterm group, greater neonatal procedural pain-related stress (adjusted for morphine) was associated with lower cortisol levels on the study day (p = .044) and lower diurnal cortisol at home (p = .023), with effects found primarily in boys. In addition, child attention problems were negatively, and thought problems were positively, associated with the cortisol response during cognitive assessment on the study day in preterm children. Our findings suggest that neonatal pain/stress contributes to altered HPA axis function up to school-age in children born very preterm, and that sex may be an important factor.
    Full-text · Article · Jan 2015 · Psychoneuroendocrinology
  • T.E. Baker · V. Lam · N. Lan · K.A. Uban · J. Weinberg

    No preview · Article · Jan 2015
  • Charlis Raineki · Aldo B. Lucion · Joanne Weinberg
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    ABSTRACT: As one of the first rodent models designed to investigate the effects of early-life experiences, the neonatal handling paradigm has helped us better understand how subtle changes in the infant environment can powerfully drive neurodevelopment of the immature brain in typical or atypical trajectories. Here, we review data from more than 50 years demonstrating the compelling effects of neonatal handling on behavior, physiology, and neural function across the lifespan. Moreover, we present data that challenge the classical view of neonatal handling as an animal model that results only in positive/beneficial outcomes. Indeed, the overall goal of this review is to offer the suggestion that the effects of early-life experiences—including neonatal handling—are nuanced rather than unidirectional. Both beneficial and negative outcomes may occur, depending on the parameters of testing, sex of the subject, and neurobehavioral system analyzed. © 2014 Wiley Periodicals, Inc. Dev Psychobiol
    No preview · Article · Dec 2014 · Developmental Psychobiology
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    ABSTRACT: Individuals with fetal alcohol spectrum disorder (FASD) are at increased risk for substance use disorders (SUD). In typically developing individuals, susceptibility to SUD is associated with alterations in dopamine and hypothalamic-pituitary-adrenal (HPA) systems, and their interactions. Prenatal alcohol exposure (PAE) alters dopamine and HPA systems, yet effects of PAE on dopamine-HPA interactions are unknown. Amphetamine-stress cross-sensitization paradigms were utilized to investigate sensitivity of dopamine and stress (HPA) systems, and their interactions following PAE. Adult Sprague-Dawley offspring from PAE, pair-fed, and ad libitum-fed control groups were assigned to amphetamine-(1-2 mg/kg) or saline-treated conditions, with injections every other day for 15 days. Fourteen days later, all animals received an amphetamine challenge (1 mg/kg) and 5 days later, hormones were measured under basal or acute stress conditions. Amphetamine sensitization (augmented locomotion, days 1-29) and cross-sensitization with acute restraint stress (increased stress hormones, day 34) were assessed. PAE rats exhibited a lower threshold for amphetamine sensitization compared to controls, suggesting enhanced sensitivity of dopaminergic systems to stimulant-induced changes. Cross-sensitization between amphetamine (dopamine) and stress (HPA hormone) systems was evident in PAE, but not in control rats. PAE males exhibited increased dopamine receptor expression (medial prefrontal cortex (mPFC)) compared to controls. PAE alters induction and expression of sensitization/cross-sensitization, as reflected in locomotor, neural, and endocrine changes, in a manner consistent with increased sensitivity of dopamine and stress systems. These results provide insight into possible mechanisms that could underlie increased prevalence of SUD, as well as the impact of widely prescribed stimulant medications among adolescents with FASD.
    Full-text · Article · Nov 2014 · Psychopharmacology
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    Joanna H. Sliwowska · Tamara S. Bodnar · Joanne Weinberg
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    ABSTRACT: Background Prenatal alcohol exposure (PAE) has adverse effects on reproductive function and hypothalamic–pituitary–gonadal (HPG) activity. Kisspeptin neurons play a role in mediating feedback effects of estradiol (E2) and progesterone (P4) on the HPG axis. We hypothesized that PAE will have long-term effects on the response of kisspeptin neurons to E2 and P4.Methods Adult female rats (53 to 58 days) from prenatal ad libitum-fed control (C), pair-fed (PF), and alcohol-exposed (PAE) groups were subjected to Sham ovariectomy (OVX) or OVX without or with replacement with low or high physiological levels of E2 and P4, and terminated under basal conditions. E2 and P4 levels, and the response of kisspeptin-ir neurons in the arcuate (ARC) and anteroventral periventricular (AVPV) nuclei to these hormones, were measured. As the E2 signal is conveyed to kisspeptin neurons via estrogen receptor-α (ER-α), we investigated PAE effects on the number of kisspeptin-ir/ER-α-ir neurons. To determine whether PAE alters interactions between kisspeptin and gonadotropin-releasing hormone (GnRH) neurons, close contacts between kisspeptin-ir fibers and GnRH-ir cell bodies were examined.ResultsOur data present the novel finding that kisspeptin-ir neurons in the ARC of PAE females show differential responses to E2 and to the combined treatment with E2 and P4 compared with controls: (i) OVX increased the number of kisspeptin-ir neurons in C and PF, but not PAE females compared with their Sham counterparts; (ii) E2 replacement restored kisspeptin-ir cell numbers to Sham levels in C and PF females but caused a robust down-regulation of kisspeptin-ir neurons below Sham levels in PAE females; (iii) OVX and replacement with high physiological concentrations of E2 resulted in fewer kisspeptin-ir cells in PAE than C females; (iv) OVX and replacement with high levels of both E2 and P4 markedly decreased the number of kisspeptin-ir neurons, below levels observed following E2 alone, in PF and C females, but had no significant effect in PAE females.Conclusions These data suggest that a possible mechanism underlying adverse effects of PAE on HPG function involves actions of alcohol on the kisspeptin system.
    Full-text · Article · Nov 2014 · Alcoholism Clinical and Experimental Research
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    ABSTRACT: Prenatal alcohol exposure (PAE) can produce a myriad of deficits. Unfortunately, affected individuals may also be exposed to the stress of an adverse home environment, contributing to deficits of attentional processes that are the hallmark of optimal executive function. Male offspring of ad-libitum-fed Control (Con), Pairfed (PF), and PAE dams were randomly assigned to either a 5-day period of variable chronic mild stress (CMS) or no CMS in adolescence. In adulthood, rats were trained in a non-match to sample task (T-maze), followed by extensive assessment in the five-choice serial reaction time task. Once rats acquired the five-choice serial reaction time task (stable accuracy), they were tested in three challenge conditions: (i) increased sustained attention, (ii) selective attention and, (iii) varying doses of d-amphetamine, an indirect dopamine and norepinephrine agonist. At birth and throughout the study, PAE offspring showed reduced body weight. Moreover, although PAE animals were similar to Con animals in task acquisition, they were progressively less proficient with transitions to shorter stimulus durations (decreased accuracy and increased omissions). Five days of adolescent CMS increased basal corticosterone levels in adolescence and disrupted cognitive performance in adulthood. Further, CMS augmented PAE-related disturbances in acquisition and, to a lesser extent, also disrupted attentional processes in Con and PF animals. Following task acquisition, challenges unmasked persistent attentional difficulties resulting from both PAE and adolescent CMS. In conclusion, PAE, adolescent CMS, and their interaction produced unique behavioural profiles that suggest vulnerability in select neurobiological processes at different stages of development.
    No preview · Article · Oct 2014 · European Journal of Neuroscience
  • Claudia Krebs · Parker Holman · Tamara Bodnar · Joanne Weinberg · Wayne Vogl

    No preview · Conference Paper · Apr 2014

Publication Stats

5k Citations
516.51 Total Impact Points


  • 2015
    • Child & Family Research Institute
      Vancouver, British Columbia, Canada
  • 1983-2015
    • University of British Columbia - Vancouver
      • • Department of Cellular and Physiological Sciences
      • • Faculty of Medicine
      • • Department of Psychology
      Vancouver, British Columbia, Canada
  • 2012
    • UBC - Universidade BRAZ CUBAS
  • 2010-2012
    • Carleton University
      • • Institute of Interdisciplinary Studies
      • • Department of Psychology
      Ottawa, Ontario, Canada
    • Centro Nacional De Investigaciones En Salud Materno Infantil (Cenismi)
      Santo Domingo Pueblo, New Mexico, United States
  • 2005-2007
    • Children's & Women's Health Centre of British Columbia
      • Department of Pediatrics
      Vancouver, British Columbia, Canada
  • 1999
    • University of Massachusetts Amherst
      Amherst Center, Massachusetts, United States