skip to main content
Idioma:

Novel Aspects of Glucocorticoid Actions

Uchoa, E. T. ; Aguilera, G. ; Herman, J. P. ; Fiedler, J. L. ; Deak, T. ; de Sousa, M. B. C.

Journal of neuroendocrinology, 2014-09, Vol.26 (9), p.557-572 [Periódico revisado por pares]

United States: Blackwell Publishing Ltd

Texto completo disponível

Citações Citado por
  • Título:
    Novel Aspects of Glucocorticoid Actions
  • Autor: Uchoa, E. T. ; Aguilera, G. ; Herman, J. P. ; Fiedler, J. L. ; Deak, T. ; de Sousa, M. B. C.
  • Assuntos: Animals ; Brain - physiology ; Eating - physiology ; feedback ; Feedback, Physiological - physiology ; food intake ; glucocorticoids ; Glucocorticoids - physiology ; HPA axis ; Hypothalamo-Hypophyseal System - physiology ; immune system ; Inflammation Mediators - physiology ; Models, Biological ; Neuronal Plasticity - physiology ; neuroplasticity ; Neurosecretory Systems - physiology ; Pituitary-Adrenal System - physiology ; Receptors, Glucocorticoid - physiology ; Receptors, Mineralocorticoid - physiology ; Stress, Physiological - physiology
  • É parte de: Journal of neuroendocrinology, 2014-09, Vol.26 (9), p.557-572
  • Notas: FAPESP
    CNPq
    National Science Foundation - No. 0822129
    ark:/67375/WNG-7JRCDB71-P
    istex:9ED94DB4536E86BBACEA0C930210C9A91F330A2F
    NIH - No. MH049698; No. MH069860
    FONDECYT - No. 1120528
    ArticleID:JNE12157
    National Institute of Child Health and Human Development
    ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-3
    content type line 23
    ObjectType-Review-2
  • Descrição: Normal hypothalamic‐pituitary‐adrenal (HPA) axis activity leading to the rhythmic and episodic release of adrenal glucocorticoids (GCs) is essential for body homeostasis and survival during stress. Acting through specific intracellular receptors in the brain and periphery, GCs regulate behaviour, as well as metabolic, cardiovascular, immune and neuroendocrine activities. By contrast to chronic elevated levels, circadian and acute stress‐induced increases in GCs are necessary for hippocampal neuronal survival and memory acquisition and consolidation, as a result of the inhibition of apoptosis, the facilitation of glutamatergic neurotransmission and the formation of excitatory synapses, and the induction of immediate early genes and dendritic spine formation. In addition to metabolic actions leading to increased energy availability, GCs have profound effects on feeding behaviour, mainly via the modulation of orexigenic and anorixegenic neuropeptides. Evidence is also emerging that, in addition to the recognised immune suppressive actions of GCs by counteracting adrenergic pro‐inflammatory actions, circadian elevations have priming effects in the immune system, potentiating acute defensive responses. In addition, negative‐feedback by GCs involves multiple mechanisms leading to limited HPA axis activation and prevention of the deleterious effects of excessive GC production. Adequate GC secretion to meet body demands is tightly regulated by a complex neural circuitry controlling hypothalamic corticotrophin‐releasing hormone (CRH) and vasopressin secretion, which are the main regulators of pituitary adrenocorticotrophic hormone (ACTH). Rapid feedback mechanisms, likely involving nongenomic actions of GCs, mediate the immediate inhibition of hypothalamic CRH and ACTH secretion, whereas intermediate and delayed mechanisms mediated by genomic actions involve the modulation of limbic circuitry and peripheral metabolic messengers. Consistent with their key adaptive roles, HPA axis components are evolutionarily conserved, being present in the earliest vertebrates. An understanding of these basic mechanisms may lead to novel approaches for the development of diagnostic and therapeutic tools for disorders related to stress and alterations of GC secretion.
  • Editor: United States: Blackwell Publishing Ltd
  • Idioma: Inglês
Links
Voltar para lista de resultados

  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

Buscando em bases de dados remotas. Favor aguardar.