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Effective early education is essential for academic achievement and positive life outcomes, particularly for children in poverty. Advances in neuroscience suggest that a focus on self-regulation in education can enhance children's engagement in learning and establish beneficial academic trajectories in the early elementary grades. Here, we experimentally evaluate an innovative approach to the education of children in kindergarten that embeds support for self-regulation, particularly executive functions, into literacy, mathematics, and science learning activities. Results from a cluster randomized controlled trial involving 29 schools, 79 classrooms, and 759 children indicated positive effects on executive functions, reasoning ability, the control of attention, and levels of salivary cortisol and alpha amylase. Results also demonstrated improvements in reading, vocabulary, and mathematics at the end of kindergarten that increased into the first grade. A number of effects were specific to high-poverty schools, suggesting that a focus on executive functions and associated aspects of self-regulation in early elementary education holds promise for closing the achievement gap.

Neuroendocrinology, the discipline concerned with how the nervous system controls hormonal secretion and how hormones control the brain, is pivotal to physiology and medicine. Neuroendocrinology has disclosed and underpins fundamental physiological, molecular biological and genetic principles such as the regulation of gene transcription and translation, the mechanisms of chemical neurotransmission and intracellular and systemic feedback control systems. Reproduction, growth, stress, aggression, metabolism, birth, feeding and drinking and blood pressure are some of the bodily functions that are triggered and/or controlled by neuroendocrine systems. In turn, neuroendocrine dysfunction due to genetic or other deficits can lead, for example, to infertility, impotence, precocious or delayed puberty, defective or excessive growth, obesity and anorexia, Cushing's Syndrome, hypertension or thyroid disorders. These as well as neuroendocrine tumors are some of the themes covered in the 36 chapters of the Handbook. Drafted by internationally acknowledged experts in the field, the Handbook chapters feature detailed up-to-date bibliographies as well as \"how do we know?\" call out sections that highlight the experimental or technical foundations for major concepts, principles, or methodological advances in each area. Aimed at senior undergraduate and graduate students, post-doctoral fellows and faculty in neuroscience, medicine, endocrinology, psychiatry, psychology and cognate disciplines, the Handbook of Neuroendocrinology satisfies an unmet need that will prove useful at the laboratory bench as well as in the office. The most comprehensive up-to-date source covering basic principles, neural regulation, hormone/brain function and behavior, and neuroendocrine pathology \"How do we know?\" callout sections highlight core conceptsHeavily illustrated with over 350 figures, 4-color throughout

ABSTRACTBackgroundPsychological stress associated with caregiving is thought to underlie the high incidence of hypertension, ischemic heart disease, and mortality, as well as reduced immune function, among caregivers of dementia patients. Here, we examined the effects of periodic leisure activities performed by caregivers of dementia patients with care recipients at home on perceived care burden and levels of stress hormones. MethodsParticipants were 42 caregivers aged ≥ 65 years of patients diagnosed with Alzheimer's dementia. They were randomly assigned to intervention and non-intervention groups. The intervention group underwent a leisure activity program (30 min/3 times/week for 24 weeks) with the care recipient, and the control group underwent normal care activities. ResultsThe Zarit Burden Interview (ZBI) score, a subjective indicator of care burden, significantly decreased after intervention in the intervention group ( p < 0.05), whereas no difference was observed in the control group. No significant changes were observed in adrenaline, noradrenaline, dopamine, and cortisol levels in both groups. ConclusionsThe lack of changes in stress hormone levels despite a decrease in subjective care burden in the intervention group might be explained by the effects of the chosen leisure activity on the neuroendocrine system. Our findings suggest that periodic leisure activities can reduce perceived care burden among caregivers of dementia patients. However, in order to evaluate accurately the effects of leisure activities of the present study, long-term follow-up of both caregivers and care recipients is necessary. The Nagoya University Department of Medicine Ethics Committee Clinical Trials Registry Number is 1290.

Effects of a Selective Serotonin Reuptake Inhibitor, Fluoxetine, on Counterregulatory Responses to Hypoglycemia in Healthy Individuals Vanessa J. Briscoe 1 , Andrew C. Ertl 1 , Donna B. Tate 1 , Sheila Dawling 2 and Stephen N. Davis 1 3 1 Department of Medicine, Vanderbilt University, Nashville, Tennessee 2 Department of Pathology, Vanderbilt University, Nashville, Tennessee 3 Veterans Affairs Medical Center, Nashville, Tennessee Corresponding author: Stephen N. Davis, steve.davis{at}vanderbilt.edu Abstract OBJECTIVE— Hypoglycemia commonly occurs in intensively-treated diabetic patients. Repeated hypoglycemia blunts counterregulatory responses, thereby increasing the risk for further hypoglycemic events. Currently, physiologic approaches to augment counterregulatory responses to hypoglycemia have not been established. Therefore, the specific aim of this study was to test the hypothesis that 6 weeks’ administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine would amplify autonomic nervous system (ANS) and neuroendocrine counterregulatory mechanisms during hypoglycemia. RESEARCH DESIGN AND METHODS— A total of 20 healthy (10 male and 10 female) subjects participated in an initial single-step hyperinsulinemic (9 pmol · kg −1 · min −1 )-hypoglycemic (means ± SE 2.9 ± 0.1 mmol/l) clamp study and were then randomized to receive 6 weeks’ administration of fluoxetine ( n = 14) or identical placebo ( n = 6) in a double-blind fashion. After 6 weeks, subjects returned for a second hypoglycemic clamp. Glucose kinetics were determined by three-tritiated glucose, and muscle sympathetic nerve activity (MSNA) was measured by microneurography. RESULTS— Despite identical hypoglycemia (2.9 ± 0.1 mmol/l) and insulinemia during all clamp studies, key ANS (epinephrine, norepinephrine, and MSNA but not symptoms), neuroendocrine (cortisol), and metabolic (endogenous glucose production, glycogenolysis, and lipolysis) responses were increased ( P < 0.01) following fluoxetine. CONCLUSIONS— This study demonstrated that 6 weeks’ administration of the SSRI fluoxetine can amplify a wide spectrum of ANS and metabolic counterregulatory responses during hypoglycemia in healthy individuals. These data further suggest that serotonergic transmission may be an important mechanism in modulating sympathetic nervous system drive during hypoglycemia in healthy individuals. Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 20 June 2008. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted June 17, 2008. Received February 18, 2008. DIABETES

The neuropeptide substance P (SP) has been supposed to be involved in the etiopathology of affective disorders, mainly because of the finding of increased levels of SP in the cerebrospinal fluid of depressed patients and the preliminary evidence of antidepressant effects of SP-receptor antagonists in depressed patients. We investigated whether SP may induce changes of sleep, mood and neuroendocrine measures that are similar to those in depressed patients. In a double-blind, randomized cross-over design, 12 healthy young men were investigated in two blocks of three consecutive nights, in which SP or NaCl was intravenously infused during the third night. Polysomnographic recordings were obtained during all nights and blood samples were drawn every 30 min during the third night. Infusion of SP caused a significant worsening of the mood of the subjects, led to an increase of REM latency and time awake during the SP-infusion intervals, caused increased stage 1 sleep in the first part of the night, and led to increased cortisol and thyroid stimulating hormone levels and a trend for decreased growth hormone levels. These effects can be interpreted as evidence for a central arousing effect of SP. Further studies should focus on the effects of substance P in patients with depressive or other psychiatric disorders.

Amphibian tadpoles display extensive anti-predator phenotypic plasticity, reducing locomotory activity and, with chronic predator exposure, developing relatively smaller trunks and larger tails. In many vertebrates, predator exposure alters activity of the neuroendocrine stress axis. We investigated predator-induced effects on stress hormone production and the mechanistic link to anti-predator defences in Rana sylvatica tadpoles. Whole-body corticosterone (CORT) content was positively correlated with predator biomass in natural ponds. Exposure to caged predators in mesocosms caused a reduction in CORT by 4 hours, but increased CORT after 4 days. Tadpoles chronically exposed to exogenous CORT developed larger tails relative to their trunks, matching morphological changes induced by predator chemical cue; this predator effect was blocked by the corticosteroid biosynthesis inhibitor metyrapone. Tadpole tail explants treated in vitro with CORT increased tissue weight, suggesting that CORT acts directly on the tail. Short-term treatment of tadpoles with CORT increased predation mortality, likely due to increased locomotory activity. However, long-term CORT treatment enhanced survivorship, likely due to induced morphology. Our findings support the hypothesis that tadpole physiological and behavioural/morphological responses to predation are causally interrelated. Tadpoles initially suppress CORT and behaviour to avoid capture, but increase CORT with longer exposure, inducing adaptive phenotypic changes.

Fifteen patients with major depression, dysthymia, or anxiety disorder with depressed mood (DSM-IV diagnoses) and 16 controls received single oral doses of 0.5mg/kg metachlorophenylpiperazine (m-CPP), a 5-HT2C agonist, and 10 mg ipsapirone, a 5-HT1A agonist, according to double-blind, placebo-controlled, cross-over design. The groups' levels of cortisol, adrenocorticotrophic hormone (ACTH) and prolactin did not differ at baseline. Both 5-HT agonists significantly elevated cortisol, ACTH, and prolactin. The cortisol response to ipsapirone was significantly blunted in major depression and dysthymia patients. Neuroendocrine responses to m-CPP did not differ between groups, but m-CPP selectively increased profile of mood states (POMS) depression and tenseness scores in patients. No effects of ipsapirone on mood were found. However, ipsapirone impaired memory performance in controls, but tended to improve memory performance in patients. The results support the evidence for both hypothalamic and possibly hippocampal 5-HT1A receptor desensitisation and non-hypothalamic, 5-HT2C receptor sensitisation, probably fronto-cortical, in patients with major depression and dysthymia.

The aryl hydrocarbon receptor (or AhR) is a cytoplasmic receptor of pollutants. It translocates into the nucleus upon binding to its ligands, and forms a heterodimer with ARNT (AhR nuclear translocator). The heterodimer is a transcription factor, which regulates the transcription of xenobiotic metabolizing enzymes. Expressed in many cells in vertebrates, it is mostly present in neuronal cell types in invertebrates, where it regulates dendritic morphology or feeding behavior. Surprisingly, few investigations have been conducted to unravel the function of the AhR in the central or peripheral nervous systems of vertebrates. In this review, we will present how the AhR regulates neural functions in both invertebrates and vertebrates as deduced mainly from the effects of xenobiotics. We will introduce some of the molecular mechanisms triggered by the well-known AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which impact on neuronal proliferation, differentiation, and survival. Finally, we will point out the common features found in mice that are exposed to pollutants, and in AhR knockout mice.

Acute stress shifts the brain into a state that fosters rapid defense mechanisms. Stress-related neuromodulators are thought to trigger this change by altering properties of large-scale neural populations throughout the brain. We investigated this brain-state shift in humans. During exposure to a fear-related acute stressor, responsiveness and interconnectivity within a network including cortical (frontoinsular, dorsal anterior cingulate, inferotemporal, and temporoparietal) and subcortical (amygdala, thalamus, hypothalamus, and midbrain) regions increased as a function of stress response magnitudes, β-adrenergic receptor blockade, but not cortisol synthesis inhibition, diminished this increase. Thus, our findings reveal that noradrenergic activation during acute stress results in prolonged coupling within a distributed network that integrates information exchange between regions involved in autonomic-neuroendocrine control and vigilant attentional reorienting.

Although it is a widely held thought that direct hormone action on peripheral tissues is sufficient to mediate the control of nutrient handling, the role of the central nervous system in certain aspects of metabolism has long been recognized. Furthermore, recent findings have suggested a more general role for the central nervous system in metabolic control, and have revealed the importance of a number of cues and hypothalamic circuits. The brain's contributions to metabolic control are more readily revealed and play a crucial part in catabolic states or in hormone deficiencies that mimic starvation.