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Neuroendocrine-Induced Immune Modulation and Autoimmunity
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Terence Smith, Adrian K. Hewson
Adrenal steroids, corticosterone in the rat and cortisol in humans, have potent effects on the neural, endocrine, and immune systems [107]. Endogenous glucocorticoids exhibit autoregulation of the HPA axis whereby excessive steroid secretion is inhibited by negative-feedback mechanisms effective at neural and pituitary levels [108,109], Hippocampal neuronal firing [110] and protein synthesis [111] are decreased and increased, respectively, whereas at the hypothalamic site, neuronal activity is reduced and CRF release and synthesis are blocked [112]. Similarly, rapid and delayed feedback effects are manifest in the anterior pituitary gland, culminating in the attenuation of ACTH secretion and synthesis [112].
Caffeine effects on locomotor and reward behavior
Published in B.S. Gupta, Uma Gupta, Caffeine and Behavior, 2020
Ernest N. Damianopoulos, Robert J. Carey
Serum corticosterone concentration (µg/ml) was determined as an index of drug-induced effects. The results are presented in the bottom panel of Figure 4.3. These results were also analyzed by a 1-way ANOVA. Group effects were again significant (F (2/39) = 7.7, p<.01. Post hoc comparison of the group means indicated that corticosterone was equally elevated in the caffeine and cocaine groups compared to that of the saline group (p<.05). These results indicate that caffeine and cocaine had a significant impact on the stress-related hormone of corticosterone, with the drug groups showing increased serum corticosterone.
Herbs with Antidepressant Effects
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
Pretreatment with silymarin also ameliorated the depression-like effects in mice caused by chronic unpredictable mild stress. Immobility was reduced in the forced swim test and preference for sucrose was restored, both of which being indications of anti-depressant effects. Treatment also reduced the high, stress-induced serum levels of corticosterone. Neurochemical analyses of brain tissue further showed that silymarin increased towards normal the levels of BDNF, and the neurotransmitters, serotonin, norepinephrine, and dopamine in the hippocampus and cerebral cortex. Levels of the inflammatory cytokines IL-6 and TNF-α were reduced in those areas of the brain; whereas signs of antioxidant effects of treatment were evident in reduced formation of malondialdehyde formation, but increases in the activities of superoxide dismutase and catalase. Chronic treatment with the antidepressant fluoxetine produced the same types of changes as silymarin.15 Along with reserpine and chronic-stressed-induced depression, silymarin also relieved the depression-like symptoms induced by acute restraint stress and olfactory bulbectomy in mice.16
Amelioration of modified chronic unpredictable stress using Celastrus paniculatus seed oil alone and in combination with fluoxetine
Published in Drug and Chemical Toxicology, 2023
Sanjana Chahuan, Sania Grover, Shamsher Singh
Besides oxidative stress and neuroinflammation, monoamine theory is of major concern in depression. It has been seen that the breakdown of monoamines (dopamine, serotonin, and norepinephrine) by enzymes like MAO and reuptake of these monoamines are blameworthy to cause depression. Therefore, to upregulate these monoamines two pharmacotherapeutic approaches are in trend, i.e., either the use of MAO inhibitors like tranylcypromine, phenelzine, or monoamine reuptake inhibitors like fluoxetine (FLU) (selective serotonin reuptake inhibitor (SSRI)), venlafaxine (selective norepinephrine reuptake inhibitor), and nefazodone (serotonin-norepinephrine reuptake inhibitor) (Fajemiroye et al. 2016). Moreover, elevated corticosterone levels are also liable for the development of depression. Hypothalamic-pituitary-adrenal (HPA) axis is supposed to play a vital role in regulating the levels of glucocorticoids through a negative feedback mechanism. But under the influence of stress, the dysregulation of this HPA axis and failure of the negative feedback mechanism takes place, resulting in high glucocorticoid (corticosterone) levels in the blood which may further leads to the genesis of depression (Ali et al. 2015).
Chronic stress decreases fertility parameters in female rats
Published in Systems Biology in Reproductive Medicine, 2023
Fahiel Casillas, Alejandra Flores-González, Lizbeth Juárez-Rojas, Alma López, Miguel Betancourt, Eduardo Casas, Iván Bahena, Edmundo Bonilla, Socorro Retana-Márquez
Corticosterone is considered the major stress hormone produced by the adrenal gland participating in the regulation of stress-induced HPA axis in rodents (Mishima et al. 2015). In the present study after stress induction, a significant increase in serum corticosterone levels was obtained in females from the stress group. In basal corticosterone levels (Aoki et al. 2010); females have a normally active HPA axis. A higher expression of corticotropin-releasing hormone (CRH) as well as an increase in the weight of the adrenal gland in female rats have been reported (Karandrea et al. 2000). In a stress condition, the release of CRH initiates HPA activation. CRF neurons in the locus coeruleus display increased CRF-1 receptor signaling and decreased CRF-1 receptor internalization in female rats. Therefore, females may be more sensitive to repeated activation of the stress response via CRF mechanisms (Bangasser et al. 2010). Also, it was reported that female rats in the proestrus phase display increased CRF expression in the paraventricular nucleus of the hypothalamus after an acute stressor (Iwasaki-Sekino et al. 2009).
The protective effect of N-acetyl cysteine against selenium toxicity and gamma irradiation in rats
Published in Drug and Chemical Toxicology, 2023
Riham Abdel-Hamid Haroun, Nahed Abdel-Aziz, Soha Saad
Corticosterone is the main adrenal corticosteroid in laboratory rodents such as rats and mice as they lack the adrenal enzyme CYP17 and therefore cannot produce cortisol (Raff and Cort 2016). Corticosterone is the main stress hormone of the glucocorticosteroid group and secreted after the activation of the hypothalamic-pituitary-adrenal axis with environmental stressors (Sokół and Koziatek-Sadłowska 2020). This is consistent with our results; as corticosterone concentration was significantly increased in the rats after the exposure of rats to different stress (toxic dose of Se and IR); but when these rats treated with NAC before toxic dose of Se and IR, it was found that corticosterone was significantly decreased, improving the protective effect of NAC. Corticosterone initiates physical response to stress by binding to glucocorticoid receptor, which is transcribed from NR3C1 gene, thus promoting stress response (Gandhi et al. 2020). Previous studies reported the increased expression level of NR3C1 gene was associated with stress such as infection and inflammation (Sevilla and Pérez 2018, Iftimovici et al. 2020), which is consistent with our results as NR3C1 expression level was significantly increased in Rad group and Se group when compared to control group; while it was decreased in Rad + NAC group and Se + NAC group when compared to Rad group and Se group, indicating the protective effect of NAC against stress. Prevatto et al. (2017) found that NAC treatment induced downregulation of NR3C1, which is in agreement with our results.