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Judy L Cameron

Publications and source records attributed to Judy L Cameron.

16 recordsLinked to original sources
PubMed2006

Economic, neurobiological, and behavioral perspectives on building America's future workforce.

A growing proportion of the U.S. workforce will have been raised in disadvantaged environments that are associated with relatively high proportions of individuals with diminished cognitive and social skills. A cross-disciplinary examination of research in economics, developmental psychology, and neurobiology reveals a striking convergence on a set of common principles that account for the potent effects of early environment on the capacity for human skill development. Central to these principles are the findings that early experiences have a uniquely powerful influence on the development of cognitive and social skills and on brain architecture and neurochemistry, that both skill development and brain maturation are hierarchical processes in which higher level functions depend on, and build on, lower level functions, and that the capacity for change in the foundations of human skill development and neural circuitry is highest earlier in life and decreases over time. These findings lead to the conclusion that the most efficient strategy for strengthening the future workforce, both economically and neurobiologically, and improving its quality of life is to invest in the environments of disadvantaged children during the early childhood years.

Adult↗
PubMed2006

Individual differences in physical activity are closely associated with changes in body weight in adult female rhesus monkeys (Macaca mulatta).

The increased prevalence of overweight adults has serious health consequences. Epidemiological studies suggest an association between low activity and being overweight; however, few studies have objectively measured activity during a period of weight gain, so it is unknown whether low activity is a cause or consequence of being overweight. To determine whether individual differences in adult weight gain are linked to an individual's activity level, we measured activity, via accelerometry, over a prolonged period (9 mo) in 18 adult female rhesus monkeys. Weight, food intake, metabolic rate, and activity were first monitored over a 3-mo period. During this period, there was mild but significant weight gain (5.5 +/- 0.88%; t =-6.3, df = 17, P < 0.0001), whereas caloric intake and activity remained stable. Metabolic rate increased, as expected, with weight gain. Activity level correlated with weight gain (r = -0.52, P = 0.04), and the most active monkeys gained less weight than the least active monkeys (t = -2.74, df = 8, P = 0.03). Moreover, there was an eightfold difference in activity between the most and least active monkeys, and initial activity of each monkey was highly correlated with their activity after 9 mo (r = 0.85, P < 0.0001). In contrast, food intake did not correlate with weight gain, and there was no difference in weight gain between monkeys with the highest vs. lowest caloric intake, total metabolic rate, or basal metabolic rate. We conclude that physical activity is a particularly important factor contributing to weight change in adulthood and that there are large, but stable, differences in physical activity among individuals.

Animals↗
PubMed2006

Increased cortisol in the cerebrospinal fluid of women with functional hypothalamic amenorrhea.

CONTEXT: The proximate cause of functional hypothalamic amenorrhea (FHA) is reduced GnRH drive. The concomitant increase in circulating cortisol suggests that psychogenic stress plays an etiologic role, but others have argued for a strictly metabolic cause, such as undernutrition or excessive exercise. Indeed, our finding that the cerebrospinal fluid (CSF) concentration of CRH was not elevated in FHA cast doubt about the extent of hypothalamic-pituitary-adrenal activation in FHA and, therefore, we wondered whether central cortisol levels were elevated. OBJECTIVE: We tested the null hypothesis that CSF cortisol levels would be comparable in FHA and eumenorrheic women (EW). DESIGN: The study is a cross-sectional comparison. SETTING: The study was set in a general clinical research center at an academic medical center. PARTICIPANTS: Fifteen women with FHA who were of normal body weight and 14 EW participated. INTERVENTION: Blood samples were collected at 15-min intervals for 24 h, followed by procurement of 25 ml CSF. MAIN OUTCOME MEASURES: Cortisol, cortisol-binding globulin (CBG), and SHBG levels in blood and CSF were the main outcome measures. RESULTS: CSF cortisol concentrations were 30% greater when serum cortisol was 16% higher in FHA compared with EW. Circulating CBG, but not SHBG, was increased in FHA and, thus, the circulating free cortisol index was similar in FHA and EW. Because CBG and SHBG were nil in CSF, the increase in CSF cortisol in FHA was unbound. CONCLUSIONS: The hypothalamic-pituitary-adrenal axis is activated in FHA. The maintenance of CRH drive despite increased CSF cortisol indicates resistance to cortisol feedback inhibition. The mechanisms mediating feedback resistance likely involve altered hippocampal corticosteroid reception and serotonergic and GABAergic neuromodulation.

Amenorrhea↗
PubMed2006

Translating research findings on early experience to prevention: animal and human evidence on early attachment relationships.

Recent studies provide a wealth of findings on the mechanisms by which early stress exposure, particularly within the early child-parent attachment relationship, may influence long-term adaptation. Translating these findings to clinical practice and social policy is now underway. In this review, some key considerations in this translational task are examined, specifically, the conceptual bases underlying the research designs, the putative mechanisms involved, and the degree to which currently available findings might shape interventions. Although the primary focus is on depression, a broader range of phenotypes associated with poor early caregiving environments is also considered.

Adaptation, Psychological↗
PubMed2005

Sensitivity to stress-induced reproductive dysfunction linked to activity of the serotonin system.

OBJECTIVE: To use a nonhuman primate model and determine whether individuals sensitive to stress-induced reproductive dysfunction have lower activity of central serotonergic neurons under nonstressed conditions. DESIGN: The activity of the central serotonergic system was assessed by measuring responsiveness to a fenfluramine challenge (5 mg/kg, IV) in sedated monkeys previously categorized as highly stress resistant (HSR; n = 4; normal menstrual cyclicity through two stress cycles), medium stress resistant (MSR; n = 5; ovulatory in the first stress cycle but anovulatory in the second stress cycle), or low stress resistant (i.e., stress sensitive, SS; n = 4; anovulatory as soon as stress is initiated). To control for differences in pituitary stores of prolactin or ACTH, the animals were subsequently administered a bolus of thyrotropin-releasing hormone (3 microg/kg) plus corticotropin releasing factor (CRF), (3 microg/kg). SETTING: Oregon National Primate Research Center, Animal Services Building. PATIENT(S): Female cynomolgus macaques exhibiting normal menstrual cycles. INTERVENTION(S): Administration of fenfluramine, a serotonin-releasing drug. MAIN OUTCOMES MEASURE(S): Serum concentrations of prolactin (PRL) and cortisol (F). RESULT(S): Prolactin release in response to fenfluramine was significantly greater in the HSR group compared with the MSR or SS groups. In contrast, cortisol was higher in the SS group compared with the other two groups. Similar responses were not evident after thyrotropin-releasing hormone + CRF stimulation. CONCLUSION(S): The lower PRL response to fenfluramine in the stress-sensitive animals suggests that stress-sensitive individuals have decreased activity in central serotonergic neurons. However, the F data suggest that the hypothalamic-pituitary-adrenal axis in stress-sensitive individuals is highly responsive to even small increases in serotonin.

Animals↗
PubMed2005

Evidence in female rhesus monkeys (Macaca mulatta) that nighttime caloric intake is not associated with weight gain.

OBJECTIVE: To evaluate the hypothesis that nighttime consumption of calories leads to an increased propensity to gain weight. RESEARCH METHODS AND PROCEDURES: Sixteen female rhesus monkeys (Macaca mulatta) were ovariectomized and placed on a high-fat diet to promote weight gain, and we examined whether monkeys that ate a high percentage of calories at night were more likely to gain weight than monkeys that ate the majority of calories during the day. RESULTS: Within 6 weeks post-ovariectomy, calorie intake and body weight increased significantly (129 +/- 14%, p = 0.04; 103 +/- 0.91%, p = 0.02, respectively). Subsequent placement on high-fat diet led to further significant increases in calorie intake and body weight (368 +/- 56%, p = 0.001; 113 +/- 4.0%, p = 0.03, respectively). However, there was no correlation between the increase in calorie intake and weight gain (p = 0.34). Considerable individual variation existed in the percentage of calories consumed at night (6% to 64% total daily caloric intake). However, the percentage of calorie intake occurring at night was not correlated with body weight (r = 0.04; p = 0.87) or weight gain (r = 0.07; p = 0.79) over the course of the study. Additionally, monkeys that showed the greatest nighttime calorie intake did not gain more weight (p = 0.94) than monkeys that showed the least nighttime calorie intake. DISCUSSION: These results show that eating at night is not associated with an increased propensity to gain weight, suggesting that individuals trying to lose weight should not rely on decreasing evening calorie intake as a primary strategy for promoting weight loss.

Animals↗
PubMed2005

Peptide YY(3-36) inhibits morning, but not evening, food intake and decreases body weight in rhesus macaques.

Peptide YY(3-36) [PYY(3-36)] is a hormone that is released after meal ingestion that is currently being investigated for the treatment of obesity; however, there are conflicting reports of the effects of PYY(3-36) on energy balance in rodent models. To shed light on this controversy, we studied the effect of PYY(3-36) on food intake and body weight in a nonhuman primate. Intravenous PYY(3-36) infusions before a morning meal transiently suppressed the rate of food intake but did not suppress the evening meal or 24-h intake. Twice-daily or continuous intravenous PYY(3-36) infusions to supraphysiological levels (levels that exceeded normal physiological levels) again suppressed the rate of feeding for the morning but not the evening meal. Twice-daily intravenous PYY(3-36) infusions for 2 weeks significantly decreased body weight in all test animals (average weight loss 1.9%) without changing insulin response to glucose infusion. These results show that endogenous PYY(3-36) may alter morning but not evening meal intake, and supraphysiological doses are required for effective suppression of food intake.

Animals↗
PubMed2004

Anxious behavior and fenfluramine-induced prolactin secretion in young rhesus macaques with different alleles of the serotonin reuptake transporter polymorphism (5HTTLPR).

Anxiety is a normal aspect of human personality, which can manifest in a variety of disorders and other negative traits. The primary treatment for anxiety is the class of drugs known as the selective serotonin reuptake inhibitors (SSRIs), which bind to the serotonin reuptake transporter. The upstream region of the gene that codes for this transporter contains a polymorphism that is an insertion/deletion event that in turn, produces long (l) and short (s) alleles in the population. This particular polymorphism in the serotonin transporter, the 5HTTLPR (serotonin transporter linked polymorphic region), is thought to be involved in the genesis of anxious traits and disorders. Most studies with human subjects have examined adult behavior, which may derive from diverse experiential and environmental backgrounds, as well as genetic differences. To better isolate the effect of genetics, we genotyped 128 infant and juvenile monkeys for the 5HTTLPR and tested for behavioral response in four testing paradigms designed to elicit fearful-anxious behaviors: a free play, remote-controlled car, human intruder, and novel fruit test. The s/s monkeys were found to be behaviorally inhibited in the free play test, engaged in more fear behaviors in the remote-controlled car test, and threatened more in the stare portion of the human intruder test, even though a small number of monkeys were assessed. There was no difference between genotypes of either sex in the prolactin response to fenfluramine. These data indicate greater anxiety in the s/s monkeys for distinct facets of anxious behavior, which are independent of a global neurohormonal challenge test. These neurobehavioral data support recent neuroimaging findings in humans indicating the importance of the 5HTTLPR for amygdala-dependent anxious behavior.

Animals↗
PubMed2004

Interrelationships between hormones, behavior, and affect during adolescence: understanding hormonal, physical, and brain changes occurring in association with pubertal activation of the reproductive axis. Introduction to part III.

This paper summarizes the goals of this section and considers current knowledge about the association between hormonal changes that occur over pubertal development and the changes in behavior and brain function over the adolescent period. It reviews the cascade of neural and hormonal changes that occur with puberty; discusses mechanisms by which these changes can affect higher-order brain processes; reviews the current limited state of knowledge about links between puberty and changes in affect regulation in the adolescent period; identifies hurdles that have made progress in our understanding of these relationships difficult; and suggests areas for future investigation that will allow us to obtain a much more comprehensive understanding of these interrelationships. This overview of the physiological processes occurring at puberty indicates that puberty (1) encompasses changes in a number of neural systems; (2) results in altered secretion of a number of hormones; (3) involves hormones that are secreted in a pulsatile manner so that collection of a single blood sample does not clearly delineate hormone profiles; and (4) shows considerable individual variation in the rate of progression and in hormone secretion during progression. The important role that gonadal steroid hormones play throughout development and adulthood in regulating plastic changes in neuronal structure and function is noted, highlighting the need for further studies to determine the extent to which the dramatic increases in circulating steroid hormones at puberty modulate brain circuits that underlie changes in social behaviors, risk-taking behaviors, and cognitive function at adolescence.

Adolescent↗
PubMed2004

Interrelationships between hormones, behavior, and affect during adolescence: complex relationships exist between reproductive hormones, stress-related hormones, and the activity of neural systems that regulate behavioral affect. Comments on part III.

Adolescence is a period in life marked by change, encompassing physiological changes associated with pubertal development, changes in social status and the social stresses that an individual faces, and changes in behavioral affect regulation. The interactions between activity in the reproductive axis, the neural systems that regulate stress, hormones produced in response to stress, and neural systems governing behavioral affect regulation are complex and multifaceted. Although our understanding of these interactions remains rudimentary, we do know that stress can suppress activity of the reproductive axis, that reproductive hormones can modulate the activity of neural systems that govern the body's responses to stress, that both reproductive function and stress responsiveness can be altered in depressed individuals, and that the function of some of the key neural systems regulating behavioral affect (i.e., serotonergic, noradrenergic, dopaminergic systems) are modulated by both gonadal steroid hormones and adrenal steroid hormones. This summary reviews the central interactions discussed in this session on the interrelationships between hormones, behavior, and affect during adolescence and identifies key topics that require further investigation in order to understand the role that pubertal changes in reproductive function, interacting with increased exposure to life stresses, play in modulating behavioral affect regulation during the adolescent period.

Adolescent↗
PubMed2004

Galanin-like peptide as a possible link between metabolism and reproduction in the macaque.

Galanin-like peptide (GALP) is a hypothalamic neuropeptide that has been implicated in the control of feeding, metabolism, and reproduction. The goal of this study was to examine the effects of central infusions of GALP on GnRH and LH secretion and to identify physiological factors that influence the expression of GALP mRNA in the brain of a primate species. Infusions of GALP into the lateral cerebroventricle of the macaque caused a significant increase in LH secretion, which was blocked by administration of the GnRH receptor antagonist acyline. However, the expression of GALP mRNA in the arcuate nucleus, as determined by in situ hybridization, was not regulated by either estradiol or progesterone. Compared with feeding ad libitum, fasting for 48 h produced a significant reduction in the hypothalamic expression of GALP mRNA. GALP neurons were found to express both neuropeptide Y Y1 receptor and serotonin 2C receptor by double-label in situ hybridization. Taken together, these results suggest that GALP neurons play a role of integrating metabolic signals, which are relayed to circuits controlling GnRH release in the macaque.

Animals↗
PubMed2003

Fasting activates neuropeptide Y neurons in the arcuate nucleus and the paraventricular nucleus in the rhesus macaque.

It is well accepted that neuropeptide Y (NPY) plays a pivotal role in the regulation of food intake and energy homeostasis in the rodent, with NPY neurons in the arcuate nucleus (ARH) being thought of as the major contributor to the complex central feeding circuitry. Recent data from our group also indicate that NPY is important in the regulation of energy homeostasis in the nonhuman primate (NHP); exogenous NPY administration into the 3rd ventricle is a potent stimulator of food intake in the male rhesus macaque. The purpose of this study was to determine if NPY neurons in the rhesus macaque respond to a metabolic challenge, induced by 48 h of fasting, in a manner similar to that seen in the rodent. NPY mRNA was detected in hypothalamic sections from 48-h fasted or fed rhesus monkeys by in situ hybridization, using a [35S]UTP-labeled riboprobe specific for human NPY. Not surprisingly, NPY mRNA was abundant in the ARH of the NHP; however, of great interest was the expression of NPY mRNA in neurons within the paraventricular nucleus of the hypothalamus (PVH) and the supraoptic nucleus (SON). This raised the question as to whether all of these populations of NPY neurons are sensitive to changes in energy availability. Indeed, NPY expression in the ARH and PVH was significantly elevated in response to fasting; however, no significant change was detected in the SON. These data indicate that the NPY neurocircuitry involved in the regulation of food intake is more complex in the NHP than in rodents.

Animals↗
PubMed2003

Heritability of fearful-anxious endophenotypes in infant rhesus macaques: a preliminary report.

BACKGROUND: Research efforts to discover the genetic underpinnings of anxiety and depression is challenging because of the etiologic heterogeneity inherent to these disorders. These efforts might be aided by the study of related behavioral phenotypes in model organisms, such as monkeys. METHODS: Eighty-five rhesus monkeys (Macaca mulatta) from the Oregon National Primate Research Center were drawn from a standard matriarchal colony and tested for behavioral response in four testing paradigms designed to elicit fearful-anxious reactions. Heritabilities were estimated using variance component-based quantitative genetic analyses with much of the genetic information arising from paternal half-sibs. RESULTS: Individual behaviors reflecting increased distress responses (e.g., vocalizations and teeth grinding) and behavioral inhibition (e.g., latency to leave mother, latency to inspect novel fruit) showed significant heritability, even though a small number of monkeys were assessed. Exploratory factor analyses identified seven clusters of behaviors across tests, some of which were found to be heritable. CONCLUSIONS: These results indicate that several specific fearful-anxious behaviors in infant rhesus monkeys are heritable within this colony. Accordingly, these phenotypes, which are believed to represent the genetic liability for anxiety and depression, are good candidates for further genetic investigation in this population.

Animals↗
PubMed2003

Growth hormone response to growth hormone-releasing hormone and clonidine in young monkeys: correlation with behavioral characteristics.

Blunted growth hormone (GH) release in response to stimulation by a secretagogue has been widely reported in both children and adults with anxiety and depressive disorders. Blunted GH responsiveness appears to be a stable characteristic of an individual, suggesting that it may be useful as a biological marker that would allow early recognition of these disease processes. Another potential biological marker for anxiety disorders is the temperamental construct of behavioral inhibition. Children identified as being behaviorally inhibited early in life are more likely than less inhibited children to suffer from anxiety disorders later in life (Biederman et al. 1993; Hirshfeld et al. 1992). If blunted GH responsiveness to pharmacological challenge and behavioral inhibition are markers of anxiety and depressive disorders, then it would follow that they would coexist in a subset of individuals. However, such prospective studies in clinically normal young children are difficult to perform. Therefore, in this study, we examined GH responsiveness and temperament in a group of 38 young rhesus monkeys (ages 3-6 months). Monkeys received an intravenous dose of 10 microg/kg of growth hormone-releasing hormone (GHRH) and 5 microg/kg of clonidine, combined, to assess GH response to stimulation. Behavioral reactivity in a fearful situation was assessed using the Human Intruder Test developed by Kalin et al. (1991). This test measures response to a potentially threatening stimulus (a human stranger making direct eye contact). Results showed a population distribution of GH response to GHRH and clonidine ranging from 120 ng/mL/90 minutes to 3,000 ng/mL/90 minutes. There was no difference in GH response in males versus females or any significant effect of age on GH response. There was a significant correlation between GH responsiveness and the time spent reacting to the intruder in the Human Intruder Test. Monkeys with lower GH responsiveness reacted less to the intruder (p < 0.01). Additionally, when monkeys were classified based on their reactivity in the Human Intruder Test, behaviorally nonreactive monkeys had significantly lower GH responsiveness than behaviorally reactive monkeys (p < 0.005). These data provide evidence that there are inherent differences in GH responsiveness to stimulation in young rhesus monkeys and that low GH responsiveness is linked to low behavioral reactivity, which may be a form of behavioral inhibition. Further studies will be necessary to determine if the characteristics of low GH responsiveness and low behavioral reactivity predict an increased propensity to develop anxious or depressive behaviors over the course of the life span.

Adrenergic alpha-Agonists↗
PubMed2002

An integrative, multidisciplinary approach to the study of brain-behavior relations in the context of typical and atypical development.

The study of brain development and that of behavioral development have historically proceeded independently of one another. This is an unfortunate set of circumstances, given that the disciplines concerned with development-for example, developmental psychology, pediatrics, psychiatry, clinical psychology, and the neurosciences-have much to learn from each other. Drawing on recent advances in the developmental brain and behavioral sciences, we illustrate the transdisciplinary approach our group has adopted in the service of uniting the research on brain and behavior in the context of development. We specifically report on our nonhuman primate and human studies that collectively illustrate our "genes to behavior" approach to the study of development. Our goal in summarizing our research in this fashion is to promote discussion about promising templates for how research on brain, behavior, and development might proceed into the 21st century.

Adolescent↗