PubMed · 10778084
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H Murase. 1999. [Corticosterone].. https://pubmed.ncbi.nlm.nih.gov/10778084/
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The present study investigated inter- and intraindividual variation of the stress response (in terms of plasma levels of corticosterone) to handling in birds. Individual captive great tits (Parus major) were exposed to a standardised capture and handling protocol three times at about 2-week intervals. Mean plasma corticosterone levels were low (<5 ng/ml) when the birds were first sampled and increased in all birds 10 min after handling (mean levels on each sampling occasion 14 to 22 ng/ml). Levels in some birds then continued to increase, whereas in other birds levels remained relatively constant or had declined 30 min after handling began. Corticosterone responses were measured three times in each bird so that variation in plasma corticosterone levels could be defined. The area under the corticosterone response curve was defined as the integrated corticosterone response and was calculated for each response curve. Variation between birds was quantified by comparing mean values of corticosterone levels and integrated corticosterone responses between birds, then calculating a coefficient of variation for the mean of the individual bird means for each corticosterone parameter. Variation within birds was quantified by calculating the mean of the coefficients of variation for each bird for each corticosterone parameter. Variation in corticosterone levels in the first blood samples at 0 min (coefficient of variation (CV) 84.0%) was greater than variation in peak levels at 10 min (CV 35.1%) and in integrated corticosterone responses (CV 31.9%), indicating that corticosterone responses were more consistent between birds than were basal corticosterone levels. This study has demonstrated that corticosterone responses to a stressor tend to be repeatable in individual great tits, and has provided a method for quantifying variation in corticosterone responses for comparison with other birds in the future.
In the present study, glycine uptake in SK-N-SH cells was determined with liquid scintillation technique, and the rapid effects of steroids on glycine uptake in SK-N-SH cells were investigated. The results were as follows. High-affinity glycine uptake in SK-N-SH cells was dependent on Na+ and Cl-. Corticosterone (CORT), progesterone (P) and dexamethasone (DEX) had rapid effects on the glycine uptake. Since estradiol (E2) and deoxycorticosterone (DOC) had no effects, it was suggested that the rapid effects of steroids were specific. The rapid effects of CORT were concentration-dependent in a range of 10(-9)-10(-6) mol/L. The rapid effects were not affected by the inhibitor of protein synthesis and persisted even when CORT was conjugated with bovine serum album, but attenuated when Ca2+ was absent in the external medium. The results suggest that the steroid effect on glycine uptake in SK-N-SH cells was nongenomicly mediated.
The activity of the hippocampus is modulated by a serotonergic projection from the midbrain. Corticosteroids regulate the activity of this raphe-hippocampal system in various ways. These effects are differentially mediated via two types of central corticosteroid receptor types, the high-affinity mineralocorticoid receptor (MR), and the lower affinity glucocorticoid receptor (GR). Under physiological fluctuations of corticosteroid concentrations, predominantly MR-mediated effects suppress the activity of the raphe-hippocampal system, notably serotonin (5-HT)1A receptor-related activity: 5-HT1A receptors are down-regulated, and the cellular response to 5-HT1A receptor activation is attenuated. Transiently increased concentrations of corticosteroids, as induced by stress, result in combined occupation of both MR and GR, and allow increased activity of the raphe-hippocampal system. Stimulatory actions of corticosteroids involving GR occupation include increased responsiveness of hippocampal neurons to 5-HT1A receptor stimulation, attenuated autoinhibition of 5-HT, and a permissive effect on stress-induced increases in 5-HT release. Under (pathological) conditions of chronically elevated corticosteroid concentrations, however, serotonergic neurotransmission is impaired. Human depression is an important example of a condition of combined hypercorticism and an apparent hypoactivity of serotonergic transmission. Deficiency of brain GR function may be genetically determined or acquired by stress. It is proposed that the balance of MR/GR activation can be altered by chronic (stress-related) changes of corticosteroid concentrations, in combination with glucocorticoid feedback resistance. Such an imbalance would lead to a relative dominance of MR-mediated suppressive effects on the activity of the raphe-hippocampal system, which may be a biologically relevant aspect of depression.