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Hormones and Behavior Sep 2021While corticosterone (CORT) is often suggested to be an important hormone regulating processes necessary for avian migration, there has been no systematic assessment of... (Review)
Review
While corticosterone (CORT) is often suggested to be an important hormone regulating processes necessary for avian migration, there has been no systematic assessment of CORT's role in migration. Prior to migration, birds increase fat stores and flight muscle size to prepare for the high energetic costs associated with long-distance flight. After attaining sufficient energetic stores, birds then make the actual decision to depart from their origin site. Once en route birds alternate between periods of flight and stopovers, during which they rest and refuel for their next bouts of endurance flight. Here, we evaluate three non-mutually exclusive hypotheses that have been proposed in the literature for CORT's role in migration. (1) CORT facilitates physiological preparations for migration [e.g. hyperphagia, fattening, and flight muscle hypertrophy]. (2) CORT stimulates departure from origin or stopover sites. (3) CORT supports sustained migratory travel. After examining the literature to test predictions stemming from each of these three hypotheses, we found weak support for a role of CORT in physiological preparation for migration. However, we found moderate support for a role of CORT in stimulating departures, as CORT increases immediately prior to departure and is higher when migratory restlessness is displayed. We also found moderate support for the hypothesis that CORT helps maintain sustained travel, as CORT is generally higher during periods of flight, though few studies have tested this hypothesis. We provide recommendations for future studies that would help to further resolve the role of CORT in migration.
Topics: Animal Migration; Animals; Corticosterone; Rest; Seasons; Songbirds
PubMed: 34273707
DOI: 10.1016/j.yhbeh.2021.105033 -
Comparative Biochemistry and... Dec 2016The recently introduced technique of measuring corticosterone in feathers currently provides the longest-term measure of corticosterone in birds. This review examines... (Review)
Review
The recently introduced technique of measuring corticosterone in feathers currently provides the longest-term measure of corticosterone in birds. This review examines the strengths, weaknesses, and unresolved technical issues of the feather corticosterone technique. Feather corticosterone's major strengths are that it provides: a retrospective assessment of corticosterone physiology, including information from absent (unseen) or dead (e.g. museum specimens) individuals; a long-term measure of corticosterone exposure over the period of feather growth (days-weeks), integrating both baseline and responses to stressors; and flexible, minimally-invasive, sampling. However, researchers considering this technique should be aware of its limitations. Feather corticosterone only reflects hormone exposure during feather growth and, when sampling during molt, corticosterone titers and ecological conditions may not be representative of the majority of the annual cycle. Synchronization of molt is often unknown for a population, requiring assumptions when making inter-individual comparisons. Additionally, unresolved technical issues include: assessing whether corticosterone is the only hormone measured by assays; determining deposition dynamics to fully understand connections between feather and plasma corticosterone titers; studying the longevity and stability of corticosterone in the feather; establishing the impact of feather size and color on corticosterone deposition; and understanding the causes and implications of corticosterone variation along the length of the feather. Notwithstanding the above limitations and technical challenges, determining corticosterone titers in feathers is proving to be a useful technique for exploring some ecological and physiological correlates in individual birds. Given the unique perspective that feather corticosterone offers, we suggest that this measure complement, not replace, plasma measurements.
Topics: Animals; Birds; Corticosterone; Feathers; Molting; Retrospective Studies; Seasons; Stress, Physiological
PubMed: 27155053
DOI: 10.1016/j.cbpa.2016.05.002 -
International Journal of Molecular... Feb 2023The aim of the experiment was to test the effect of an elevated level of glucocorticoids on the mouse hippocampal transcriptome after 12 h of treatment with...
The aim of the experiment was to test the effect of an elevated level of glucocorticoids on the mouse hippocampal transcriptome after 12 h of treatment with corticosterone that was administered during an active phase of the circadian cycle. Additionally, we also tested the circadian changes in gene expression and the decay time of transcriptomic response to corticosterone. Gene expression was analyzed using microarrays. Obtained results show that transcriptomic responses to glucocorticoids are heterogeneous in terms of the decay time with some genes displaying persistent changes in expression during 9 h of rest. We have also found a considerable overlap between genes regulated by corticosterone and genes implicated previously in stress response. The examples of such genes are , , , , , , , , , , , , , , , , , , , , , , , , , , , , , and . This indicates that the applied model is a useful tool for the investigation of mechanisms underlying the stress response.
Topics: Mice; Animals; Corticosterone; Glucocorticoids; Hippocampus; Gene Expression Profiling; Transcriptome
PubMed: 36769150
DOI: 10.3390/ijms24032828 -
Physiology & Behavior Apr 2022Stress hormones such as cortisol play a critical role in depressive disorders. Therefore, corticosterone has been used to develop a depression model in animals. Our...
Stress hormones such as cortisol play a critical role in depressive disorders. Therefore, corticosterone has been used to develop a depression model in animals. Our previous studies found that the precursor of brain-derived neurotrophic factor (proBDNF) and its receptors are upregulated in depression in human and animal models. In the present study, we aimed to examine whether proBDNF and mature BDNF (mBDNF) are altered in the corticosterone-induced depression model in mice. Male and female mice were given corticosterone dissolved in 0.3% hydroxypropyl- β-cyclodextrin (β-CD) or vehicle (β-CD) in drinking water for 33 days. We have found that corticosterone induced depressive-like behaviours as reflected by increased immobility time in the tail suspension test and decreased grooming time in the splash test. Corticosterone also induced anxiety-like behaviours as represented by decreased entries into the central zone of the open field test and the open arms of the elevated plus maze test. We found that corticosterone administration resulted in differential changes of proBDNF and mature BDNF in different brain regions and peripheral tissues. ProBDNF was increased in the hippocampus and cerebellum, but no change was found in the prefrontal cortex and hypothalamus. Both proBDNF and mBDNF were significantly increased in the pituitary gland. In contrast, proBDNF was significantly decreased in the adrenal gland. There were no significant changes in proBDNF or mBDNF in other peripheral tissues, including the liver and sex organs. We conclude that the stress hormone corticosterone causes depressive behaviours but differentially regulates the processing of proBDNF in mice. ProBDNF may participate in the development of depression behaviours in corticosterone treated animals.
Topics: Affect; Animals; Brain-Derived Neurotrophic Factor; Corticosterone; Female; Hippocampus; Male; Mice; Prefrontal Cortex
PubMed: 35074305
DOI: 10.1016/j.physbeh.2022.113721 -
Molecular and Cellular Endocrinology Jul 2022The coordinated proliferation and apoptosis of granulosa cells plays a critical role in follicular development. To identify the exact mechanisms of how stress-driven...
Corticosterone triggers anti-proliferative and apoptotic effects, and downregulates the ACVR1-SMAD1-ID3 cascade in chicken ovarian prehierarchical, but not preovulatory granulosa cells.
The coordinated proliferation and apoptosis of granulosa cells plays a critical role in follicular development. To identify the exact mechanisms of how stress-driven glucocorticoid production suppresses reproduction, granulosa cells were isolated from chicken follicles at different developmental stages and then treated with corticosterone. Using CCK-8, EDU and TUNEL assays, we showed that corticosterone could trigger both anti-proliferative and pro-apoptotic effects in granulosa cells from 6 to 8 mm follicles only, while depicting no influence on granulosa cells from any preovulatory follicles. High-throughput transcriptomic analysis identified 1362 transcripts showing differential expression profiles in granulosa cells from 6 to 8 mm follicles after corticosterone treatment. Interestingly, Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that 17 genes were enriched in the TGF-β signaling pathway, and 13 showed differential expression patterns consistent with corticosterone-induced effects. The differential expression profiles of these 13 genes were examined by quantitative real-time PCR in cultured chicken ovarian granulosa cells at diverse developmental stages following corticosterone challenge for a short (8 h) or long period (24 h). After 24 h of treatment, INHBB, FST, FMOD, NOG, ACVR1, SMAD1 and ID3 were the genes that responded consistently with corticosterone-induced proliferative and apoptotic events in all granulosa cells detected. However, only ACVR1, SMAD1 and ID3 could initiate coincident expression patterns after being treated for 8 h, suggesting their significance in corticosterone-mediated actions. Collectively, these findings indicate that corticosterone can inhibit proliferation and cause apoptosis in chicken ovarian prehierarchical, but not preovulatory granulosa cells, through impeding ACVR1-SMAD1-ID3 signaling presumptively.
Topics: Animals; Apoptosis; Chickens; Corticosterone; Female; Granulosa Cells; Ovarian Follicle
PubMed: 35577112
DOI: 10.1016/j.mce.2022.111675 -
Steroids Jan 2022Testicular steroidogenesis is depressed by adrenal-secreted corticosterone (CORT) under stress. However, the mechanisms are not well understood. This study investigated...
Testicular steroidogenesis is depressed by adrenal-secreted corticosterone (CORT) under stress. However, the mechanisms are not well understood. This study investigated the details of testicular steroidogenesis depression during fasting. Blood levels of adrenocorticotropic hormone secreted from the pituitary glands increased, but blood CORT was not changed in rats that fasted for 96 h, in spite of the rats being severely stressed. CORT in fasting adult male rats increased more than three times in the testis, but reduced testicular testosterone (T) and blood T levels to 5% and 2% of the control, respectively, was observed. The contents of T precursor (except PGN) were drastically reduced in the fasted-rat testes. Testicular CORT levels were elevated, but the enzymatic activity of cytochrome P45011β, which produces CORT, remained unchanged. The enzymatic activities of 3β-hydroxysteroid dehydrogenase (3β-HSD), mediating the conversion of pregnenolone to progesterone, decreased in the fasted-rat testes. Thus, fasting suppressed testicular steroidogenesis by affecting the enzyme activity of 3β-HSD in the testes and drastically reduced T and increased CORT synthesis. It can be considered that T synthesis involved in cell proliferation is suppressed due to lack of energy during fasting. Conversely, 11β-hydroxylase enzyme activity was induced and CORT synthesis is increased to cope with the fasting stress. Hence, it can be concluded that CORT synthesis in the testes plays a role in the local defense response.
Topics: Animals; Corticosterone; Fasting; Male; Rats; Rats, Sprague-Dawley; Stress, Physiological; Testis
PubMed: 34843801
DOI: 10.1016/j.steroids.2021.108947 -
Life Sciences 1989Corticosterone possesses two distinctly opposite metabolic actions. The actions are strictly dose-dependent and are linked to type I and type II corticosteroid receptor...
Corticosterone possesses two distinctly opposite metabolic actions. The actions are strictly dose-dependent and are linked to type I and type II corticosteroid receptor binding. These conclusions are drawn from continuous infusion studies where corticosterone yields a bitonic dose-response curve for body weight gain and feeding efficiency. Anabolic at low serum levels, corticosterone concentrations above 2 micrograms/dl bring about an opponent catabolic process that intensifies and eventually masks the anabolic action. Relatively pure type I (aldosterone) and type II (RU28362 and dexamethasone) corticosterone receptor agonists produce opposite monotonic functions that respectively mimic the ascending and descending arms of the corticosterone dose-response curve. Stimulation of either receptor increases the proportion of carcass fat to lean body mass by either increasing carcass lipids (type I) or by reducing protein (type II).
Topics: Aldosterone; Androstanols; Animals; Body Weight; Corticosterone; Dexamethasone; Dose-Response Relationship, Drug; Drug Implants; Eating; Infusion Pumps, Implantable; Male; Rats; Rats, Inbred Strains; Receptors, Glucocorticoid
PubMed: 2796609
DOI: 10.1016/0024-3205(89)90026-x -
Physiology & Behavior Jun 2023This study investigated the interactive effect of glucocorticoid and Gamma-aminobutyric acid (GABA) receptors in the Infralimbic (IL) cortex on fear extinction in rats'...
Corticosterone injection into the infralimbic prefrontal cortex enhances fear memory extinction: Involvement of GABA receptors and the extracellular signal-regulated kinase.
This study investigated the interactive effect of glucocorticoid and Gamma-aminobutyric acid (GABA) receptors in the Infralimbic (IL) cortex on fear extinction in rats' auditory fear conditioning task (AFC). Animals received 3 conditioning trial tones (conditioned stimulus, 30 s, 4 kHz, 80 dB) co-terminated with a footshock (unconditioned stimulus, 0.8 mA, 1 s). Extinction testing was conducted over 3 days (Ext 1-3) after conditioning. Intra-IL injection of corticosterone (CORT, 20 ng/0.3 µl/side) was performed 15 min before the first extinction trial (Ext 1) which attenuated auditory fear expression in subsequent extinction trials (Ext 1-3), demonstrating fear memory extinction enhancement. Co-injection of the GABA agonist muscimol (250 ng/0.3 µl/side) or the GABA agonist baclofen (250 ng/0.3 µl/side) 15 min before corticosterone, did not significantly affect the facilitative effects of corticosterone on fear extinction. However, co-injection of the GABA antagonist bicuculline (BIC, 100 ng/0.3 µl/side) or the GABA antagonist CGP35348 (CGP, 100 ng/0.3 µl/side) 15 min before corticosterone, blocked the facilitative effects of corticosterone on fear extinction. Moreover, extracellular signal-regulated kinase (ERK) and cAMP response element-binding (CREB) in the IL were examined by Western blotting analysis after the first extinction trial (Ext 1) in some groups. Intra-IL injection of corticosterone increased the ERK activity but not CREB. Co-injection of the bicuculline or CGP35348 blocked the enhancing effect of corticosterone on ERK expression in the IL. Glucocorticoid receptors (GRs) activation in the IL cortex by corticosterone increased ERK activity and facilitated fear extinction. GABA or GABA antagonists decreased ERK activity and inhibited corticosterone's effect. GRs and GABA receptors in the IL cortex jointly modulate the fear extinction processes via the ERK pathway. This pre-clinical animal study may highlight GRs and GABA interactions in the IL cortex modulating fear memory processes in fear-related disorders such as post-traumatic stress disorder (PTSD).
Topics: Rats; Animals; Glucocorticoids; Corticosterone; Extinction, Psychological; Extracellular Signal-Regulated MAP Kinases; Receptors, GABA; Fear; Bicuculline; Rats, Sprague-Dawley; Prefrontal Cortex; Receptors, Glucocorticoid; gamma-Aminobutyric Acid
PubMed: 36918107
DOI: 10.1016/j.physbeh.2023.114156 -
Psychoneuroendocrinology Mar 2022Circadian rhythms play a prominent role in psychiatric health with disruption in rhythms associated with poor mental health. Corticosterone (CORT) is an important...
Circadian rhythms play a prominent role in psychiatric health with disruption in rhythms associated with poor mental health. Corticosterone (CORT) is an important hormone in entraining the biological rhythms of many cells throughout the body and coordinating peripheral rhythms with the central master clock. Here, we tested the hypothesis that excess CORT during the circadian trough would lead to a flattening of period genes (Per1 and Per2) rhythms in limbic brain areas, and thus impact emotional behaviors. Male rats were injected daily with 2.5 mg/kg CORT or vehicle for 21 days at either ZT0 or ZT12 and sucrose preference, open field, and forced swim behaviors measured during the dark phase of the light cycle. After three weeks of injections, a reduction in sucrose preference was observed in animals injected with CORT at ZT0 and the reduction significantly correlated with reductions in Per2 mRNA expression in the central amygdala (CeA) and bed nucleus of the stria terminalis (BNST). No changes in behavior or period gene expression were observed in animals injected with CORT at ZT12. DsiRNA was used to directly reduce Per2 levels in either the CeA or BNST and behavior was assessed. Despite reductions in Per2 expression in the CeA, no behavioral changes were observed. In contrast, a reduction in Per2 expression in the BNST was sufficient to reduce sucrose preference. The results demonstrate that CORT significantly contributes to the circadian expression of Period genes in certain limbic brain areas and disruption in diurnal CORT or Per2 expression can lead to impaired emotional behavioral responses.
Topics: Amygdala; Animals; Circadian Rhythm; Corticosterone; Male; Period Circadian Proteins; Rats; Sucrose
PubMed: 34952453
DOI: 10.1016/j.psyneuen.2021.105628 -
Viruses Feb 2023Despite the benefits of combinatorial antiretroviral therapies (cART), virotoxic HIV proteins are still detectable within the central nervous system. Approximately half...
Despite the benefits of combinatorial antiretroviral therapies (cART), virotoxic HIV proteins are still detectable within the central nervous system. Approximately half of all cART-treated patients contend with neurological impairments. The mechanisms underlying these effects likely involve virotoxic HIV proteins, including glycoprotein 120 (gp120). Glycoprotein-120 is neurotoxic due to its capacity to activate microglia. Corticosterone has been found to attenuate neuronal death caused by gp120-induced microglial cytokine production . However, the concentration-dependent effects of corticosterone on microglial activation states and the associated behavioral outcomes are unclear. Herein, we conducted parallel in vitro and in vivo studies to assess gp120-mediated effects on microglial activation, motor function, anxiety- and depression-like behavior, and corticosterone's capacity to attenuate these effects. We found that gp120 activated microglia in vitro, and corticosterone attenuated this effect at an optimal concentration of 100 nM. Transgenic mice expressing gp120 demonstrated greater anxiety-like behavior on an elevated plus maze, and a greater duration of gp120 exposure was associated with motor deficits and anxiety-like behavior. Circulating corticosterone was lower in gp120-expressing males and diestrous females. Greater circulating corticosterone was associated with reduced anxiety-like behavior. These findings may demonstrate a capacity for glucocorticoids to attenuate gp120-mediated neuroinflammation and anxiety-like behavior.
Topics: Female; Male; Mice; Animals; Corticosterone; Microglia; Anxiety; Mice, Transgenic; Glycoproteins
PubMed: 36851638
DOI: 10.3390/v15020424