About: Corticosterone is a(n) research topic. Over the lifetime, 12965 publication(s) have been published within this topic receiving 530105 citation(s). The topic is also known as: 11beta,21-dihydroxyprogesterone & 17-deoxycortisol.
Papers published on a yearly basis
TL;DR: It is suggested that maternal behavior serves to "program" hypothalamic-pituitary-adrenal responses to stress in the offspring.
Abstract: Variations in maternal care affect the development of individual differences in neuroendocrine responses to stress in rats. As adults, the offspring of mothers that exhibited more licking and grooming of pups during the first 10 days of life showed reduced plasma adrenocorticotropic hormone and corticosterone responses to acute stress, increased hippocampal glucocorticoid receptor messenger RNA expression, enhanced glucocorticoid feedback sensitivity, and decreased levels of hypothalamic corticotropin-releasing hormone messenger RNA. Each measure was significantly correlated with the frequency of maternal licking and grooming (all r 9s > −0.6). These findings suggest that maternal behavior serves to “program” hypothalamic-pituitary-adrenal responses to stress in the offspring.
TL;DR: The balance in actions mediated by the two corticosteroid receptor types in these neurons appears critical for neuronal excitability, stress responsiveness, and behavioral adaptation and Dysregulation of this MR/GR balance brings neurons in a vulnerable state with consequences for regulation of the stress response and enhanced vulnerability to disease in genetically predisposed individuals.
Abstract: In this review, we have described the function of MR and GR in hippocampal neurons. The balance in actions mediated by the two corticosteroid receptor types in these neurons appears critical for neuronal excitability, stress responsiveness, and behavioral adaptation. Dysregulation of this MR/GR balance brings neurons in a vulnerable state with consequences for regulation of the stress response and enhanced vulnerability to disease in genetically predisposed individuals. The following specific inferences can be made on the basis of the currently available facts. 1. Corticosterone binds with high affinity to MRs predominantly localized in limbic brain (hippocampus) and with a 10-fold lower affinity to GRs that are widely distributed in brain. MRs are close to saturated with low basal concentrations of corticosterone, while high corticosterone concentrations during stress occupy both MRs and GRs. 2. The neuronal effects of corticosterone, mediated by MRs and GRs, are long-lasting, site-specific, and conditional. The action depends on cellular context, which is in part determined by other signals that can activate their own transcription factors interacting with MR and GR. These interactions provide an impressive diversity and complexity to corticosteroid modulation of gene expression. 3. Conditions of predominant MR activation, i.e., at the circadian trough at rest, are associated with the maintenance of excitability so that steady excitatory inputs to the hippocampal CA1 area result in considerable excitatory hippocampal output. By contrast, additional GR activation, e.g., after acute stress, generally depresses the CA1 hippocampal output. A similar effect is seen after adrenalectomy, indicating a U-shaped dose-response dependency of these cellular responses after the exposure to corticosterone. 4. Corticosterone through GR blocks the stress-induced HPA activation in hypothalamic CRH neurons and modulates the activity of the excitatory and inhibitory neural inputs to these neurons. Limbic (e.g., hippocampal) MRs mediate the effect of corticosterone on the maintenance of basal HPA activity and are of relevance for the sensitivity or threshold of the central stress response system. How this control occurs is not known, but it probably involves a steady excitatory hippocampal output, which regulates a GABA-ergic inhibitory tone on PVN neurons. Colocalized hippocampal GRs mediate a counteracting (i.e., disinhibitory) influence. Through GRs in ascending aminergic pathways, corticosterone potentiates the effect of stressors and arousal on HPA activation. The functional interaction between these corticosteroid-responsive inputs at the level of the PVN is probably the key to understanding HPA dysregulation associated with stress-related brain disorders. 5. Fine-tuning of HPA regulation occurs through MR- and GR-mediated effects on the processing of information in higher brain structures. Under healthy conditions, hippocampal MRs are involved in processes underlying integration of sensory information, interpretation of environmental information, and execution of appropriate behavioral reactions. Activation of hippocampal GRs facilitates storage of information and promotes elimination of inadequate behavioral responses. These behavioral effects mediated by MR and GR are linked, but how they influence endocrine regulation is not well understood. 6. Dexamethasone preferentially targets the pituitary in the blockade of stress-induced HPA activation. The brain penetration of this synthetic glucocorticoid is hampered by the mdr1a P-glycoprotein in the blood-brain barrier. Administration of moderate amounts of dexamethasone partially depletes the brain of corticosterone, and this has destabilizing consequences for excitability and information processing. 7. The set points of HPA regulation and MR/GR balance are genetically programmed, but can be reset by early life experiences involving mother-infant interaction. 8. (ABSTRACT TRUNCATED)
TL;DR: The purpose of the present study was to reinvestigate the role of the central retinal projections in neuroendocrine regulation and find that lesions in the suprachiasmatic region of the hypothalamus abolish the constant estrous response to light in the female rat.
Abstract: The role of vision in neuroendocrine regulation is well-known1, 2, but few data are available on specific visual pathways mediating such functions or their relation to brain centers controlling rhythmic events. Two sets of observations are pertinent to these problems. First, selective ablation of the inferior accessory optic tracts in the rat eliminates the response of the pineal melatonin-forming enzyme, hydroxyindole-Omethyltransferase (HIOMT) to light, without affecting visually guided behavioral responses, whereas section of the primary optic tracts causes a loss of visual behavior with preservation of the pineal HIOMT response to light 3-5. Second, Critchlow 6 has found that lesions in the suprachiasmatic region of the hypothalamus abolish the constant estrous response to light in the female rat, a response that is maintained after section of the primary optic tracts. His observations are of particular interest in view of the recent demonstration of a direct retinohypothalamic projection terminating in the suprachiasmatic nuclei in the rat v. The purpose of the present study was to reinvestigate the role of the central retinal projections in neuroendocrine regulation. In the studies noted above, only prolonged responses to continuous lighting conditions were examined. The experiments reported here were directed toward a different function, the neural regulation of a true circadian rhythm exemplified by the diurnal variation in adrenal corticosterone content1, 6. Two experiments were performed. The subjects for each were female albino rats (Holtzman Co., Madison, Wis.) weighing approximately 180-200 g at the beginning of the experiment. Female rats were used in these experiments because theirdiurnal rhythm in adrenal corticosterone content has a greater amplitude than that of males 6. They were housed in clear plastic cages (6-8 per cage) with free access to food and water. The cages were in racks illuminated by fluorescent lamps (Vita-Lite, Duro-Test Corp.) with a light emission similar to that of natural light. The animals were exposed to approximately 50 ft.-cd of illumination during the 12 h (07.00 to 19.00) the lights were on each day. All surgical procedures were performed under ether anesthesia. The animals were sacrificed on the 21st postoperative day at 4 time points around the clock, 07.09, 13.00, 19.00 and 24.00 hours. Their adrenals were removed and frozen on dry ice prior to subsequent analysis for corticosterone content using a modification of the method of Silber s. The location of each brain lesion was verified by histologic study. In the first experiment 4 groups of animals were used. One was subjected to sham operation and a second to blinding by bilateral orbital enucleation. Visual pathway lesions were placed in the final two groups. In the first of these a lesion was made unilaterally to destroy the optic tract just beyond its emergence from the chiasm (stereotaxic coordinates; anterior 7 ram, lateral 1.5 mm, ventral 2.5 mm below horizontal zero with the tooth bar 5 mm above the ear bars) by passing anodal DC current of 3 mA for 60 sec through an insulated electrode. The eye ipsilateral to the lesion was then removed so that the only intact visual pathways in these animals were the retinohypothalamic projection and one uncrossed primary optic tract. Because of
TL;DR: Exposure to microbes at an early developmental stage is required for the HPA system to become fully susceptible to inhibitory neural regulation, and results suggest that commensal microbiota can affect the postnatal development of the Hpa stress response in mice.
Abstract: Indigenous microbiota have several beneficial effects on host physiological functions; however, little is known about whether or not postnatal microbial colonization can affect the development of brain plasticity and a subsequent physiological system response. To test the idea that such microbes may affect the development of neural systems that govern the endocrine response to stress, we investigated hypothalamic–pituitary–adrenal (HPA) reaction to stress by comparing germfree (GF), specific pathogen free (SPF) and gnotobiotic mice. Plasma ACTH and corticosterone elevation in response to restraint stress was substantially higher in GF mice than in SPF mice, but not in response to stimulation with ether. Moreover, GF mice also exhibited reduced brain-derived neurotrophic factor expression levels in the cortex and hippocampus relative to SPF mice. The exaggerated HPA stress response by GF mice was reversed by reconstitution with Bifidobacterium infantis. In contrast, monoassociation with enteropathogenic Escherichia coli, but not with its mutant strain devoid of the translocated intimin receptor gene, enhanced the response to stress. Importantly, the enhanced HPA response of GF mice was partly corrected by reconstitution with SPF faeces at an early stage, but not by any reconstitution exerted at a later stage, which therefore indicates that exposure to microbes at an early developmental stage is required for the HPA system to become fully susceptible to inhibitory neural regulation. These results suggest that commensal microbiota can affect the postnatal development of the HPA stress response in mice.
TL;DR: The presence of the enzyme 11 beta-hydroxy-steroid dehydrogenase, which converts cortisol and corticosterone, but not aldosterone, to their 11-keto analogs, means that these analogs cannot bind to mineralocorticoid receptors.
Abstract: Mineralocorticoid receptors, both when in tissue extracts and when recombinant-derived, have equal affinity for the physiological mineralocorticoid aldosterone and for the glucocorticoids cortisol and corticosterone, which circulate at much higher concentrations than aldosterone. Such receptors are found in physiological mineralocorticoid target tissues (kidney, parotid, and colon) and in nontarget tissues such as hippocampus and heart. In mineralocorticoid target tissues the receptors are selective for aldosterone in vivo because of the presence of the enzyme 11 beta-hydroxy-steroid dehydrogenase, which converts cortisol and corticosterone, but not aldosterone, to their 11-keto analogs. These analogs cannot bind to mineralocorticoid receptors.