Neuroendocrinology of social behavior
Female; Male; Behavior; Animals; Social Behavior; Hypothalamo-Hypophyseal System/physiology; Neurosecretory Systems/physiology; Animal; Neuropeptides/physiology; Arvicolinae/physiology; Finches/physiology; Gonadal Steroid Hormones/physiology; Oxytocin/physiology; Pair Bond
Discovering the hormonal and neural mechanisms that promote affiliative social behavior is a high priority in behavioral neuroscience. Although studies with standard laboratory rodents have afforded many important insights, exciting advances are also occurring through comparative research with nonstandard species that vary in sociality or form socially monogamous pair bonds, work that is often informed by an explicitly evolutionary perspective. Research with prairie voles has examined the roles of sex steroid hormones, adrenal glucocorticoids, oxytocin family peptides, and dopamine in the formation of monogamous pairs. Corticosterone facilitates pairing by males but inhibits it in females, vasopressin (acting via the V1a receptor) and oxytocin facilitate pairing, and dopamine in the nucleus accumbens also facilitates pairing. Research with zebra finches is testing the limits of generality of these mechanisms, and has shown how sex steroid effects early in life along with social experience lead to an adult's sex preference in a pairing partner. Estrogen manipulations during the embryonic or nestling periods result in females that prefer to pair with other females. An all-female social environment can reinforce such effects, and can also produce males and females that will pair with either sex. Research with multiple species of estrildid finches is revealing the contributions of peptidergic and dopaminergic mechanisms to the evolution of species differences in whether animals are gregarious or territorial. Mechanisms for and responses to vasotocin (avian vasopressin) in the septal region of the brain are predicted by sociality in this group of birds.
2009
Adkins-Regan E
ILAR 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/10.1093/ilar.50.1.5" target="_blank" rel="noreferrer">10.1093/ilar.50.1.5</a>
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>
Associations between the neuroendocrine and immune systems
Humans; Animals; Biomarkers of Pain; Cell Communication; Cytokines/physiology; Hormones/physiology; Hypothalamo-Hypophyseal System/physiology; Immune System/physiology; Interleukins/physiology; Leukocytes/physiology; Neurosecretory Systems/physiology; Signal Transduction
Organisms respond to infection with complex adaptations involving bidirectional communication between the immune and neuroendocrine systems. The idea of intercellular communication between the neuroendocrine and immune systems via common signal molecules has provided a conceptual framework for such crosstalk. The studies to date show that cells of the immune system contain receptors for neuroendocrine hormones and can also be considered a source of pituitary and hypothalamic peptides. The structure and pattern of synthesis of these peptides by leukocytes appear similar to neuroendocrine hormones, although some differences exist. Once secreted, these peptide hormones may function as endogenous regulators of the immune system as well as conveyors of information from the immune to the neuroendocrine system. The plasma hormone concentrations contributed by lymphocytes usually do not reach the levels required when the pituitary gland is the source, but because immune cells are mobile, they have the potential to locally deposit the hormone at the target site. Likewise, other studies show that cells of the neuroendocrine system contain receptors for cytokines and can also be considered a source of cytokines, particularly interleukin-1 (IL-1) and IL-6. In the pituitary IL-1 beta coexists with thyroid stimulating hormone in a subpopulation of thyrotropes, suggesting it may have a role as a pituitary paracrine factor. The cytokines, including IL-1, IL-2, IL-6, interferon-gamma, and tumor necrosis factor, exert profound effects on hypothalamic pituitary axes. It is our hypothesis that the relay of information to the neuroendocrine system represents a sensory function for the immune system wherein leukocytes recognize stimuli that are not recognizable by the central and peripheral nervous systems (i.e., bacteria, tumors, viruses, and antigens). The recognition of such noncognitive stimuli by immunocytes is then converted into information and a physiological change occurs. Future studies into the physiological role that cytokines and neuroendocrine hormones have in these systems will be of considerable interest for both immunologists and endocrinologists.
1995
Weigent DA; Blalock JE
Journal Of Leukocyte Biology
1995
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/10.1002/jlb.58.2.137" target="_blank" rel="noreferrer">10.1002/jlb.58.2.137</a>