Neuroendocrine Responses (neuroendocrine + response)

Distribution by Scientific Domains


Selected Abstracts


The Medial Amygdala Modulates Body Weight but not Neuroendocrine Responses to Chronic Stress

JOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2010
M. B. Solomon
Stress pathologies such as depression and eating disorders (i.e. anorexia nervosa) are associated with amygdalar dysfunction, which are linked with hypothalamic-pituitary-adrenal axis (HPA) axis hyperactivity. The medial amygdaloid nucleus (MeA), a key output nucleus of the amygdaloid complex, promotes HPA axis activation to acute psychogenic stress and is in a prime position to mediate the deleterious effects of chronic stress on physiology and behaviour. The present study tests the hypothesis that the MeA is necessary for the development of maladaptive physiological changes caused by prolonged stress exposure. Male rats received bilateral ibotenate or sham lesions targeting the MeA and one half underwent 2 weeks of chronic variable stress (CVS) or served as home cage controls. Sixteen hours post CVS, all animals were exposed to an acute restraint challenge. CVS induced thymic involution, adrenal hypertrophy, and attenuated body weight gain and up-regulation of hypothalamic corticotrophin-releasing hormone mRNA expression. Consistent with previous literature, lesions of the MeA dampened stress-induced increases in corticosterone after 30 min of exposure to acute restraint stress. However, this effect was independent of CVS exposure, suggesting that the MeA may not be critical for modulating neuroendocrine responses after chronic HPA axis drive. Interestingly, lesion of the MeA modestly exaggerated the stress-induced attenuation of weight gain. Overall, the data obtained suggest that the MeA modulates the neuroendocrine responses to acute but not chronic stress. In addition, the data suggest that the MeA may be an important neural component for the control of body weight in the face of chronic stress. [source]


Oestrogen Receptor , is Essential for Female-Directed Chemo-Investigatory Behaviour but is not Required for the Pheromone-Induced Luteinizing Hormone Surge in Male Mice

JOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2000
S. R. Wersinger
The expression of normal masculine sexual behaviour requires testosterone. Testosterone can bind to androgen receptors, either in its native form, or after reduction to other androgen metabolites. In addition, testosterone can be aromatized to oestrogen, and bind to oestrogen receptor , and/or ,. Male copulatory behaviour is deficient in mice lacking functional oestrogen receptor , gene (ER,KO mice). We sought to determine which aspect(s) of masculine sexual behaviour is compromised in the ER,KOs. Specifically, we asked whether ER,KO males have reduced motivation and/or an inability to recognize oestrous females. We found significant differences between mice of different genotypes in the amount of chemo-investigatory behaviour displayed and in the target of their investigation. Wild-type males spent more time investigating ovariectomized, oestradiol-treated females, than either males, or ovariectomized females that had not received hormone priming. ER,KO males spent little time investigating any of the stimulus mice and showed no preferences. To test the hypothesis that this lack of chemo-investigatory behaviour is due to the inability of ER,KO males to detect and respond to female pheromones, we exposed males to chemosensory cues (soiled bedding) from females. Males resided in clean, or female-soiled, cage bedding for 60 min. Next, blood was collected and plasma luteinizing hormone (LH) assayed. We also assessed Fos-like immunoreactivity (Fos-ir) in several neural regions involved in processing chemosensory cues. Despite the fact that male ER,KOs spend little time engaged in chemo-investigation of females, their neuroendocrine responses to female-soiled bedding were similar to those seen in wild-type males. Our data suggest that the normal coupling between the neuroendocrine response to females and the generation of sexual behaviour is disrupted in ER,KO mice. Responses to female pheromones do not require ER,. However, normal male sexual performance requires the ER, gene. [source]


Breastfeeding and Maternal Stress Response and Health

NUTRITION REVIEWS, Issue 7 2004
Elizabeth Sibolboro Mezzacappa Ph.D.
This article reviews findings on the maternal stress and health effects of lactation. Several significant associations have emerged. Compared with not breastfeeding, breastfeeding is associated with increased parasympathetic nervous system modulation, greater vascular stress response, lower perceived stress levels, and fewer depressive symptoms. Breastfeeding exclusively is associated with an attenuated initial sympathetic cardiac nervous system response to some laboratory stressors. Bottle-feeding is associated with increased sympathetic and decreased parasympathetic cardiac control. The act of breastfeeding is associated with decreased neuroendocrine response to stressors and decreased negative mood. Finally, breastfeeding is associated with enhanced physical and mental health compared with non-breastfeeding. [source]


Corticosteroids and the cardiovascular response to stress: a pilot study of the 35% CO2 challenge in Addison's disease

CLINICAL ENDOCRINOLOGY, Issue 3 2006
J. M. Kaye
Summary Objective, Glucocorticoids play an essential role in the neuroendocrine response to stress, influencing both the hypothalamic,pituitary,adrenal (HPA) axis and the sympatho-adrenomedullary (SAM) axis at several levels. In this pilot study, a clinical model of primary adrenocortical failure (Addison's disease, AD) has been used to evaluate the role of circulating glucocorticoids in both the autonomic and psychological response to stress. Design and subjects, Five subjects with known AD underwent a randomized, double-blind, placebo-controlled investigation in which they received fixed glucocorticoid plus mineralocorticoid hormone replacement or placebo for 48 h prior to a 35% CO2 challenge. Measurement, Psychological responses immediately before and after CO2 exposure were assessed by questionnaire. Systolic blood pressure (SBP) and heart rate were measured automatically at 1-min intervals for 5 min before and 5 min after the CO2 exposure. Results, While on hormone replacement, all subjects had an identical response to CO2 to that recorded in normal volunteers (initial bradycardia, an increase in blood pressure and subjective feelings of anxiety). On no replacement, however, the bradycardia and anxiety responses were not significantly altered, but the pressor response was markedly attenuated (+156 5 mmHg on replacement compared with +42 33 mmHg off replacement; P = 0043). Conclusions, These data provide further evidence that the CO2 -induced bradycardia is a direct , presumably parasympathetic , response to CO2 independent of the pressor effect, and that the pressor response itself is dependent on the presence of the circulating corticosteroid. [source]


Forearm vascular and neuroendocrine responses to graded water immersion in humans

ACTA PHYSIOLOGICA, Issue 2 2000
Gabrielsen
The hypothesis that graded expansion of central blood volume by water immersion to the xiphoid process and neck would elicit a graded decrease in forearm vascular resistance was tested. Central venous pressure increased (P < 0.05) by 4.2 0.4 mmHg (mean SEM) during xiphoid immersion and by 10.4 0.5 mmHg during neck immersion. Plasma noradrenaline was gradually suppressed (P < 0.05) by 62 8 and 104 11 pg mL,1 during xiphoid and neck immersion, respectively, indicating a graded suppression of sympathetic nervous activity. Plasma concentrations of arginine vasopressin were suppressed by 1.5 0.5 pg mL,1 (P < 0.05) during xiphoid immersion and by 2.0 0.5 pg mL,1 during neck immersion (P < 0.05 vs. xiphoid immersion). Forearm subcutaneous vascular resistance decreased to the same extent by 26 9 and 28 4% (P < 0.05), respectively, during both immersion procedures, whereas forearm skeletal muscle vascular resistance declined only during neck immersion by 27 6% (P < 0.05). In conclusion, graded central blood volume expansion initiated a graded decrease in sympathetic nervous activity and AVP-release. Changes in forearm subcutaneous vascular resistance, however, were not related to the gradual withdrawal of the sympathetic and neuroendocrine vasoconstrictor activity. Forearm skeletal muscle vasodilatation exhibited a more graded response with a detectable decrease only during immersion to the neck. Therefore, the forearm subcutaneous vasodilator response reaches saturation at a lower degree of central volume expansion than that of forearm skeletal muscle. [source]


The vomeronasal organ is required for the expression of lordosis behaviour, but not sex discrimination in female mice

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2006
Matthieu Keller
Abstract The role of the vomeronasal organ (VNO) in mediating neuroendocrine responses in female mice is well known; however, whether the VNO is equally important for sex discrimination is more controversial as evidence exists for a role of the main olfactory system in mate recognition. Therefore, we studied the effect of VNO removal (VNOx) on the ability of female mice to discriminate between volatile and non-volatile odours of conspecifics of the two sexes and in different endocrine states using Y-maze tests. VNOx female mice were able to reliably distinguish between male and female or male and gonadectomized (gdx) male volatile odours. However, when subjects had to discriminate between male and female or gdx male non-volatile odours, VNOx females were no longer able to discriminate between sex or different endocrine status. These results thus show that the VNO is primarily involved in the detection and processing of non-volatile odours, and that female mice can use volatile odours detected and processed by the main olfactory system for mate recognition. However, VNO inputs are needed to promote contact with the male, including facilitation of lordosis responses to his mounts. A single subcutaneous injection with gonadotropin-releasing hormone (GnRH) partially reversed the deficit in lordosis behaviour observed in VNOx females suggesting that VNO inputs may reach hypothalamic GnRH neurons to influence the display of sexual behaviour. [source]


Marker-assisted dissection of genetic influences on motor and neuroendocrine sensitization to cocaine in rats

GENES, BRAIN AND BEHAVIOR, Issue 3 2009
L. F. Vendruscolo
This study investigated genetic influences on behavioral and neuroendocrine responses to cocaine sensitization. We used male and female rats of the inbred strains Lewis (LEW) and spontaneously hypertensive rats (SHR), which display genetic differences in stress-related responses. The influence of two quantitative trait loci (QTL; Ofil1 and Ofil2 on chromosomes 4 and 7), which modulate stress reactivity in rats, on the effects of cocaine was also investigated through the use of recombinant lines (derived from a LEW SHR intercross) selected by their genotype at Ofil1 and Ofil2. Animals were given repeated cocaine or saline injections and tested for locomotion (induction of sensitization). Two weeks later, all animals were challenged with cocaine, and locomotion and corticosterone levels were measured (expression of sensitization). Results indicated that male SHR rats showed more behavioral sensitization than LEW rats, whereas no strain differences in sensitization were seen among females. When challenged with cocaine, LEW and SHR rats of both sexes pretreated with cocaine showed behavioral sensitization compared with saline pretreated animals; however, only LEW rats displayed an increase in the corticosterone levels. Ofil1 was found to influence the induction of sensitization in males and Ofil2 modulated the locomotor effect of cocaine in females. This study provides evidence of a genotype-dependent relationship between the induction and expression of cocaine sensitization, and between the behavioral and neuroendocrine responses induced by cocaine. Moreover, the Ofil1 and Ofil2 loci may contain one or more genes that control the behavioral effects of cocaine in rats. [source]


The Medial Amygdala Modulates Body Weight but not Neuroendocrine Responses to Chronic Stress

JOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2010
M. B. Solomon
Stress pathologies such as depression and eating disorders (i.e. anorexia nervosa) are associated with amygdalar dysfunction, which are linked with hypothalamic-pituitary-adrenal axis (HPA) axis hyperactivity. The medial amygdaloid nucleus (MeA), a key output nucleus of the amygdaloid complex, promotes HPA axis activation to acute psychogenic stress and is in a prime position to mediate the deleterious effects of chronic stress on physiology and behaviour. The present study tests the hypothesis that the MeA is necessary for the development of maladaptive physiological changes caused by prolonged stress exposure. Male rats received bilateral ibotenate or sham lesions targeting the MeA and one half underwent 2 weeks of chronic variable stress (CVS) or served as home cage controls. Sixteen hours post CVS, all animals were exposed to an acute restraint challenge. CVS induced thymic involution, adrenal hypertrophy, and attenuated body weight gain and up-regulation of hypothalamic corticotrophin-releasing hormone mRNA expression. Consistent with previous literature, lesions of the MeA dampened stress-induced increases in corticosterone after 30 min of exposure to acute restraint stress. However, this effect was independent of CVS exposure, suggesting that the MeA may not be critical for modulating neuroendocrine responses after chronic HPA axis drive. Interestingly, lesion of the MeA modestly exaggerated the stress-induced attenuation of weight gain. Overall, the data obtained suggest that the MeA modulates the neuroendocrine responses to acute but not chronic stress. In addition, the data suggest that the MeA may be an important neural component for the control of body weight in the face of chronic stress. [source]


Rhythm-Dependent Light Induction of the c-fos Gene in the Turkey Hypothalamus

JOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2007
A. Thayananuphat
Day length (photoperiod) is a powerful synchroniser of seasonal changes in the reproductive neuroendocrine activity in temperate-zone birds. When exposed to light during the photoinducible phase, reproductive neuroendocrine responses occur. However, the neuroendocrine systems involved in avian reproduction are poorly understood. We investigated the effect of light exposure at different circadian times upon the hypothalamus and components of the circadian system, using c-fos mRNA expression, measured by in situ hybridisation, as an indicator of light-induced neuronal activity. Levels of c-fos mRNA in these areas were compared after turkey hens (on a daily 6-h light period) had been exposed to a 30-min period of light occurring at 8, 14, or 20 h after the onset of first light of the day (subjective dawn). Non-photostimulated control birds were harvested at the same times. In birds, photostimulated within the photoinducibile phase (14 h), in contrast to before or after, c-fos mRNA was significantly increased in the nucleus commissurae pallii (nCPa), nucleus premamillaris (PMM), eminentia mediana (ME), and organum vasculosum lamina terminalis (OVLT). Photostimulation increased c-fos mRNA expression in the pineal gland, nucleus suprachiasmaticus, pars visualis (vSCN) and nucleus inferioris hypothalami compared to that of their corresponding nonphotostimulated controls. However, the magnitudes of the responses in these areas were similar irrespective of where in the dark period the pulses occurred. No c-fos mRNA was induced in the nucleus infundibulari, in response to the 30-min light period at any of the circadian times tested. The lack of c-fos up-regulation in the pineal gland and vSCN following photostimulation during the photoinducible phase lends credence to the hypothesis that these areas are not involved in the photic initiation of avian reproduction. On the other hand, c-fos mRNA increases in the nCPa, ME, and OVLT support other studies showing that these areas are involved in the onset of reproductive behaviour initiated by long day lengths. The present study provides novel data showing that the PMM in the caudal hypothalamus is involved in the neuronally mediated, light-induced initiation of reproductive activity in the turkey hen. [source]


Changes in Hypothalamic-Pituitary-Adrenal Function, Body Temperature, Body Weight and Food Intake with Repeated Social Stress Exposure in Rats

JOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2006
S. Bhatnagar
Abstract These present studies aimed to compare changes in hypothalamic-pituitary-adrenal (HPA) activity and body temperature in response to acute social defeat, to repeated social stress and to novel restraint after repeated stress, as well as to assess effects on metabolic parameters by measuring body weight gain and food and water intake. We found that social defeat produced a marked increase in both adrenocorticotrophic hormone and corticosterone compared to placement in a novel cage. Similarly, body temperature was also increased during social defeat and during 30 min of recovery from defeat. We then examined the effects of 6 days of repeated social stress and observed minimal HPA responses to repeated social stress compared to control rats. These neuroendocrine responses were contrasted by robust increases in body temperature during stress and during recovery from stress during 6 days of repeated stress. However, in response to novel restraint, repeatedly stressed rats displayed facilitated body temperature responses compared to controls, similar to our previous findings with HPA activity. Food intake was increased during the light period during which defeat took place, but later intake during the dark period was not affected. Repeated stress decreased body weight gain in the dark period but food intake was increased overall during the 6 days of repeated stress in the light period. As a result, repeated stress increased cumulative food intake during the light period in the stressed rats but these relatively small increases in food intake were unable to prevent the diminished total weight gain in repeatedly stressed rats. Overall, the results demonstrate that, although acute social defeat has similar effects on temperature and HPA activity, repeated exposure to social stress has divergent effects on HPA activity compared to body temperature and that dampened weight gain produced by repeated social stress cannot be fully explained by changes in food intake. [source]


Oestrogen Receptor , is Essential for Female-Directed Chemo-Investigatory Behaviour but is not Required for the Pheromone-Induced Luteinizing Hormone Surge in Male Mice

JOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2000
S. R. Wersinger
The expression of normal masculine sexual behaviour requires testosterone. Testosterone can bind to androgen receptors, either in its native form, or after reduction to other androgen metabolites. In addition, testosterone can be aromatized to oestrogen, and bind to oestrogen receptor , and/or ,. Male copulatory behaviour is deficient in mice lacking functional oestrogen receptor , gene (ER,KO mice). We sought to determine which aspect(s) of masculine sexual behaviour is compromised in the ER,KOs. Specifically, we asked whether ER,KO males have reduced motivation and/or an inability to recognize oestrous females. We found significant differences between mice of different genotypes in the amount of chemo-investigatory behaviour displayed and in the target of their investigation. Wild-type males spent more time investigating ovariectomized, oestradiol-treated females, than either males, or ovariectomized females that had not received hormone priming. ER,KO males spent little time investigating any of the stimulus mice and showed no preferences. To test the hypothesis that this lack of chemo-investigatory behaviour is due to the inability of ER,KO males to detect and respond to female pheromones, we exposed males to chemosensory cues (soiled bedding) from females. Males resided in clean, or female-soiled, cage bedding for 60 min. Next, blood was collected and plasma luteinizing hormone (LH) assayed. We also assessed Fos-like immunoreactivity (Fos-ir) in several neural regions involved in processing chemosensory cues. Despite the fact that male ER,KOs spend little time engaged in chemo-investigation of females, their neuroendocrine responses to female-soiled bedding were similar to those seen in wild-type males. Our data suggest that the normal coupling between the neuroendocrine response to females and the generation of sexual behaviour is disrupted in ER,KO mice. Responses to female pheromones do not require ER,. However, normal male sexual performance requires the ER, gene. [source]


Increased Cortisol Response to Surgery in Patients With Alcohol Problems Who Developed Postoperative Confusion

ALCOHOLISM, Issue 8 2004
Akira Kudoh
Background: Patients with alcohol problems often develop postoperative confusion and have impaired cortisol, ACTH, and norepinephrine. However, the relationship between neuroendocrine responses to surgical stress and postoperative confusion remains unclear in patients with alcohol problems. Methods: Plasma cortisol, ACTH, and norepinephrine concentrations during and after surgery in 30 patients with alcohol problems and 30 control patients who underwent lower abdominal surgery were measured before the induction of anesthesia, 15 and 60 min after skin incision, 60 min after the end of surgery, the next day, and the second day after the operation. Results: Plasma cortisol concentrations (21.2 4.7 ,gdl,1) of patients with alcohol problems before anesthesia were significantly higher than 15.6 4.8 ,gdl,1 of control patients. Plasma cortisol and ACTH responses to surgery in patients with alcohol problems were not significantly increased compared with preoperative values. The incidence of postoperative confusion was significantly higher in patients with alcohol problems than that of control patients (33% vs. 3%). Plasma cortisol concentrations (29.7 7.0, 31.2 6.6, 30.3 8.0, and 28.4 6.2 ,gdl,1) 15 and 60 min after the skin incision, 60 min after the end of surgery, and the next day after operation in postoperatively confused patients with alcohol problems were significantly higher than those of nonconfused patients with alcohol problems (23.0 5.8, 22.7 4.1, 22.4 7.2, and 21.9 5.5 ,gdl,1). Conclusion: The cortisol response to surgical stress increases in patients with alcohol problems who develop postoperative confusion, although cortisol response to surgical stress decreases in patients with alcohol problems without postoperative confusion. [source]