Neurobiological mechanisms in major depressive disorder
Child; Humans; Psychotherapy; Environment; Depressive Disorder; Stress; Receptors; Atrophy; Hypothalamo-Hypophyseal System/physiology; Psychological/psychology; Genetic; Pituitary-Adrenal System/physiology; Polymorphism; Antidepressive Agents/therapeutic use; Brain-Derived Neurotrophic Factor/genetics; Brain/metabolism/pathology; Child Behavior/psychology; Corticotropin-Releasing Hormone/blood; Dopamine/genetics; Dopamine/metabolism; Major/genetics/metabolism/therapy; Serotonin Plasma Membrane Transport Proteins/genetics; Serotonin/metabolism
2009
aan het Rot M; Mathew SJ; Charney DS
Canadian Medical Association Journal
2009
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1503/cmaj.080697" target="_blank" rel="noreferrer">10.1503/cmaj.080697</a>
Stress and the adolescent brain
Humans; Stress; adolescent; Biomarkers of Pain; Brain/physiology; Hypothalamo-Hypophyseal System/physiology; Pituitary-Adrenal System/physiology; Psychological/physiopathology; Puberty/physiology
During adolescence the brain shows remarkable changes in both structure and function. The plasticity exhibited by the brain during this pubertal period may make individuals more vulnerable to perturbations, such as stress. Although much is known about how exposure to stress and stress hormones during perinatal development and adulthood affect the structure and function of the brain, relatively little is known about how the pubertal brain responds to stress. Furthermore, it is not clear whether stressors experienced during adolescence lead to altered physiological and behavioral potentials in adulthood, as has been shown for perinatal development. The purpose of this review is to present what is currently known about the pubertal maturation of the hypothalamic-pituitary-adrenal (HPA) axis, the neuroendocrine axis that mediates the stress response, and discuss what is currently known about how stressors affect the adolescent brain. Our dearth of knowledge regarding the effects of stress on the pubertal brain will be discussed in the context of our accumulating knowledge regarding stress-induced neuronal remodeling in the adult. Finally, as the adolescent brain is capable of such profound plasticity during this developmental stage, we will also explore the possibility of adolescence as a period of interventions and opportunities to mitigate negative consequences from earlier developmental insults.
2006
Romeo RD; McEwen BS
Annals Of The New York Academy Of Sciences
2006
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1196/annals.1376.022" target="_blank" rel="noreferrer">10.1196/annals.1376.022</a>
Peripheral opioid receptors mediating antinociception in inflammation. Activation by endogenous opioids and role of the pituitary-adrenal axis
Male; Analysis of Variance; Animals; Rats; Biomarkers of Pain; Dose-Response Relationship; Drug; Receptors; Naloxone/pharmacology; Foot; Biomarkers Reference List; Adrenalectomy; Cold; Endorphins/physiology; Hypophysectomy; Inbred Strains; Inflammation/physiopathology; Naltrexone/pharmacology; Nociceptors/physiopathology; Opioid/physiology; Pituitary-Adrenal System/physiology; Stress/physiopathology; Swimming
This study investigated the involvement of endogenous opioid peptides in mediating cold water swim (CWS) stress-induced antinociception (SIA) in rats with unilateral hind paw inflammation induced by Freund's complete adjuvant (FCA). Following 0.5, 1 and 2 min of CWS, there was a duration-dependent elevation of paw pressure threshold (PPT) in both inflamed and non-inflamed paws which was maximal immediately after CWS and returned to control values within 15 min. The antinociception elicited in the inflamed paw was significantly greater than that elicited in the non-inflamed paw. The antinociception induced by a 1 min CWS was dose dependently antagonized by tertiary naloxone (0.125-1 mg/kg s.c.) and completely reversed by tertiary naltrexone (0.5 mg/kg). Quaternary naltrexone (5-40 mg/kg s.c.) was similarly effective in reversing the elevation of inflamed PPT induced by a 1 min CWS stress. In contrast, similar doses of quaternary naltrexone had no effect against centrally mediated morphine antinociception in non-inoculated rats. Adrenalectomy was without effect on the pattern of SIA seen in FCA-treated rats. Surgical hypophysectomy completely abolished the differential antinociception induced by 0.5 and 1 min durations of CWS but had little effect on that following 2 min of CWS stress. Inhibition of hypophysial corticotrophic cell secretion with dexamethasone (300 micrograms/kg) injected s.c. 120 min prior to CWS completely abolished the differential SIA at all durations of CWS tested. beta-Endorphin 12.5 micrograms/kg administered i.v. in non-stressed rats also caused a greater elevation of PPT in inflamed than in non-inflamed paws. This effect was not reversed by concomitant i.v. administration of (-) tertiary naloxone 5 mg/kg or quaternary naltrexone 20 mg/kg.
1990
Parsons CG; Czlonkowski A; Stein C; Herz A
Pain
1990
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/0304-3959(90)91112-v" target="_blank" rel="noreferrer">10.1016/0304-3959(90)91112-v</a>
Pituitary-adrenal function and hypothalamic beta-endorphin release in vitro following food deprivation
Male; Time Factors; Animals; Rats; Non-U.S. Gov't; Research Support; Body Weight; Blood Glucose/metabolism; Corticosterone/blood; In Vitro; Pituitary-Adrenal System/physiology; Adrenal Glands/physiology; beta-Endorphin/secretion; Corticotropin-Releasing Hormone/pharmacology; Dexamethasone/pharmacology; Food Deprivation; Hypothalamus/drug effects/secretion; Organ Size; Thymus Gland/physiology; Wistar
Basal and dexamethasone-suppressed adrenal glucocorticoid secretion and hypothalamic beta-endorphin (BE) release in vitro were investigated in rats deprived of food for 24, 48, 72, and 96 h. Fasting for up to 48 h neither caused significant changes in serum corticosterone levels nor in the suppressive effect of dexamethasone. Food deprivation for 72-96 h resulted in increased basal serum corticosterone, diminished suppression by dexamethasone, and a significant involution of the thymus. Basal in vitro BE release from hypothalamic explants was significantly increased after the first day of food deprivation, and in vitro perifusion with corticotropin-releasing hormone (CRH) failed to enhance BE release further. With continuing food deprivation, basal BE release remained significantly greater than that from hypothalami originating from normally fed control rats. The stimulatory effect of CRH on BE release was only partially restored after 2 days of fasting. The results suggest that food deprivation for more than 2 days increases basal glucocorticoid secretion, and signs of impairment in hypothalamic-pituitary-adrenal regulation become apparent. These findings might be implicated in the pathogenetic mechanisms of endocrine dysregulation in diseases related to caloric reduction.
1993
Mitev Y; Almeida OF; Patchev V
Brain Research Bulletin
1993
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/0361-9230(93)90033-8" target="_blank" rel="noreferrer">10.1016/0361-9230(93)90033-8</a>