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Corticosterone Treatment (corticosterone + treatment)
Selected AbstractsElevated corticosterone levels in stomach milk, serum, and brain of male and female offspring after maternal corticosterone treatment in the ratDEVELOPMENTAL NEUROBIOLOGY, Issue 10 2010Susanne Brummelte Abstract Early influences such as maternal stress affect the developmental outcome of the offspring. We created an animal model of postpartum depression/stress based on giving high levels of corticosterone (CORT) to the rat dam, which resulted in behavioral and neural changes in the offspring. This study investigated whether highly elevated levels of maternal CORT during pregnancy or the postpartum result in higher levels of CORT in the stomach milk, serum, and brain of offspring. Dams received daily injections of CORT (40 mg/kg) or oil (control) either during pregnancy (gestational days 10,20) or the postpartum (Days 2,21). Pups that were exposed to high gestational maternal CORT had higher CORT levels in serum, but not in stomach milk or brain, on postnatal day (PND) 1. However, on PND7, pups that were exposed to high postpartum maternal CORT had higher CORT levels in stomach milk and brain, but not in serum. Conversely on PND18, pups that were exposed to high postpartum maternal CORT had higher CORT levels in serum, but not in brain (prefrontal cortex, hypothalamus, or hippocampus). Moreover, 24 h after weaning, there were no significant differences in serum CORT levels between the groups. Thus, CORT given to the dam during pregnancy or the postpartum results in elevated levels of CORT in the offspring, but in an age- and tissue-dependent manner. Developmental exposure to high CORT could reprogram the HPA axis and contribute to the behavioral and neural changes seen in adult offspring. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 70: 714,725, 2010 [source] Regulation of MCP-1 production in brain by stress and noradrenaline-modulating drugsJOURNAL OF NEUROCHEMISTRY, Issue 2 2010Jose L. M. Madrigal J. Neurochem. (2010) 113, 543,551. Abstract While it is accepted that noradrenaline (NA) reduction in brain contributes to the progression of certain neurodegenerative diseases, the mechanisms through which NA exerts its protective actions are not well known. We previously reported that NA induced production of monocyte chemoattractant protein (MCP-1/CCL2) in cultured astrocytes mediated some of the neuroprotective actions of NA. We have now examined the regulation of MCP-1 production in vivo. Treatment of mice with the NA precursor l -threo-3,4-dihydroxyphenylserine induced the production of MCP-1 in astrocytes. In contrast, exposure to stress (a process known to elevate brain NA levels) produced only a moderate increase of MCP-1 because of the inhibitory activity of glucocorticoids released during the stress response. Similarly, corticosterone treatment of astrocytes caused a reduction of constitutive as well as the NA-induced MCP-1 production. When stressed rats had the production of glucocorticoids blocked by the selective inhibitor metyrapone, a large increase of MCP-1 concentration was observed in cortex, whereas propranolol (a beta adrenergic receptor blocker) avoided modifications of MCP-1 after stress. Desipramine (an inhibitor of NA reuptake) also caused an increase of MCP-1 in cortex. These data suggest that some phenomena caused by the alteration of NA or glucocorticoids could be mediated by MCP-1. [source] Roles of Corticotropin-Releasing Factor, Neuropeptide Y and Corticosterone in the Regulation of Food Intake In Xenopus laevisJOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2004E. J. Crespi Abstract In mammals, hypothalamic control of food intake involves counterregulation of appetite by anorexigenic peptides such as corticotropin-releasing factor (CRF), and orexigenic peptides such as neuropeptide Y (NPY). Glucocorticoids also stimulate food intake by inhibiting CRF while facilitating NPY actions. To gain a better understanding of the diversity and evolution of neuroendocrine feeding controls in vertebrates, we analysed the effects of CRF, NPY and glucocorticoids on food intake in juvenile Xenopus laevis. We also analysed brain CRF and NPY mRNA content and plasma corticosterone concentrations in relation to nutritional state. Intracerebroventricular (i.c.v.) injection of ovine CRF suppressed food intake while CRF receptor antagonist ,helical CRF(9,41) significantly increased food intake relative to uninjected and placebo controls. By contrast, i.c.v. injection of frog NPY and short-term corticosterone treatment increased food intake. Semi-quantitative reverse transcription-polymerase chain reaction analyses showed that CRF and NPY mRNA fluctuated with food intake in the brain region containing the mid-posterior hypothalamus, pretectum, and optic tectum: CRF mRNA decreased 6 h after a meal and remained low through 31 days of food deprivation; NPY mRNA content also decreased 6 h after a meal, but increased to prefeeding levels by 24 h. Plasma corticosterone concentration increased 6 h after a meal, returned to prefeeding levels by 24 h, and did not change with prolonged food deprivation. This postprandial increase in plasma corticosterone may be related to the subsequent increase in plasma glucose and body water content that occurs 24 h postfeeding. Overall, our data support the conclusion that, similar to other vertebrates, CRF is anorexigenic while NPY is orexigenic in X. laevis, and CRF secretion modulates food intake in the absence of stress by exerting an inhibitory tone on appetite. Furthermore, the stress axis is activated in response to food intake, but in contrast to mammals and birds is not activated during periods of food deprivation. [source] Effect of Corticosteroid Treatment In Vitro on Adrenalectomy-Induced Impairment of Synaptic Transmission in the Rat Dentate GyrusJOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2000Stienstra Removal of the rat adrenals results after 3 days in the appearance of apoptotic cells in the dentate gyrus. Apoptosis is accompanied by an impaired synaptic transmission in the dentate gyrus. Substitution in vivo with a low dose of corticosterone was found to prevent both the appearance of apoptotic cells and the functional impairment. In the present study we determined whether the functional normalisation after corticosterone treatment critically depends on prevention of apoptosis. To address this question, brain slices from rats showing apoptosis after adrenalectomy were treated in vitro with the mineralocorticoid aldosterone (3 nM) or with 30 nM corticosterone, which is assumed to activate both mineralo- and glucocorticoid receptors. Steroids were briefly applied either during recording (acute effects) or several hours before recording (long-term effects). While the slope of the fEPSP recorded in the outer molecular layer of the dentate gyrus in response to perforant path stimulation was not affected up to 1 h after acute administration of the steroids, fEPSP slopes recorded 2.5,3 h after corticosterone or aldosterone treatment were significantly increased, to the level of the sham-operated controls. The results indicate that delayed corticosteroid effects through in vitro activation of mineralocorticoid receptors (MRs) are sufficient to normalise synaptic transmission in the dentate gyrus of ADX rats, even in the presence of apoptotic cells. We tentatively conclude that the impaired synaptic transmission seen after ADX is probably not primarily caused by the appearance of apoptotic cells. [source] The effect of ,two hit' neonatal and young-adult stress on dopaminergic modulation of prepulse inhibition and dopamine receptor densityBRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2009Kwok Ho Christopher Choy Background and purpose:, A combination of early neurodevelopmental insult(s) and young-adult stress exposure may be involved in the development of schizophrenia. We studied prepulse inhibition (PPI) regulation in rats after an early stress, maternal deprivation, combined with a later stress, simulated by chronic corticosterone treatment, and also determined whether changes in brain dopamine receptor density were involved. Experimental approach:, Rats were subjected to either 24 h maternal deprivation on postnatal day 9, corticosterone treatment from 8 to 10 weeks of age, or both. At 12 weeks of age, the rats were injected with 0.1, 0.3 or 1.0 mg·kg,1 of apomorphine or 0.5 or 2.5 mg·kg,1 of amphetamine and PPI was determined using automated startle boxes. Dopamine D1 and D2 receptor levels were assessed in the nucleus accumbens and caudate nucleus using receptor autoradiography. Key results:, Young-adult treatment with corticosterone resulted in attenuated disruption of PPI by apomorphine and amphetamine. In some rats, maternal deprivation resulted in reduced baseline PPI which added to the effect of corticosterone treatment. There was no down-regulation of dopamine D1 or D2 receptors. Conclusions and implications:, These results confirm and extend our finding of an inhibitory interaction of developmental stress on dopaminergic regulation of PPI. No corresponding changes in dopamine receptor density were observed in brain regions with a major involvement in PPI regulation, suggesting long-lasting desensitization of dopamine receptor signalling or indirect changes in PPI regulation. [source] | |||||||||||||