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Stressed Rats (stressed + rat)
Selected AbstractsChanges in Hypothalamic-Pituitary-Adrenal Function, Body Temperature, Body Weight and Food Intake with Repeated Social Stress Exposure in RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2006S. Bhatnagar Abstract These present studies aimed to compare changes in hypothalamic-pituitary-adrenal (HPA) activity and body temperature in response to acute social defeat, to repeated social stress and to novel restraint after repeated stress, as well as to assess effects on metabolic parameters by measuring body weight gain and food and water intake. We found that social defeat produced a marked increase in both adrenocorticotrophic hormone and corticosterone compared to placement in a novel cage. Similarly, body temperature was also increased during social defeat and during 30 min of recovery from defeat. We then examined the effects of 6 days of repeated social stress and observed minimal HPA responses to repeated social stress compared to control rats. These neuroendocrine responses were contrasted by robust increases in body temperature during stress and during recovery from stress during 6 days of repeated stress. However, in response to novel restraint, repeatedly stressed rats displayed facilitated body temperature responses compared to controls, similar to our previous findings with HPA activity. Food intake was increased during the light period during which defeat took place, but later intake during the dark period was not affected. Repeated stress decreased body weight gain in the dark period but food intake was increased overall during the 6 days of repeated stress in the light period. As a result, repeated stress increased cumulative food intake during the light period in the stressed rats but these relatively small increases in food intake were unable to prevent the diminished total weight gain in repeatedly stressed rats. Overall, the results demonstrate that, although acute social defeat has similar effects on temperature and HPA activity, repeated exposure to social stress has divergent effects on HPA activity compared to body temperature and that dampened weight gain produced by repeated social stress cannot be fully explained by changes in food intake. [source] Effects of escitalopram on the regulation of brain-derived neurotrophic factor and nerve growth factor protein levels in a rat model of chronic stressJOURNAL OF NEUROSCIENCE RESEARCH, Issue 11 2009Olaf Schulte-Herbrüggen Abstract Escitalopram (ES-CIT) is a widely used, highly specific antidepressant. Until now there has been very little evidence on how this drug under pathological conditions affects an important feature within the pathophysiology of stress-related disorders such as depression: the endogenous neurotrophins. By using a well-characterized rat model in which chronic stress induces depressive-like behavior, the levels of neurotrophins brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were determined in representative brain regions and serum using a highly sensitive improved fluorometric two-site ELISA system. There was a significant increase of BDNF in the left and right cortices after stress treatment (twofold increase) that was reversed by application of ES-CIT. An ES-CIT-dependent NGF reduction in stressed rats was detectable in the right cortex only (P = 0.027). The left hippocampus revealed significantly higher amounts of BDNF (2.5-fold increase) protein than the right hippocampus. These interhemispheric differences were unrelated to stress or ES-CIT treatment in all animals. BDNF and NGF of the frontal cortex, cerebellum, and serum did not change between the study groups. There was a negative correlation between body weight and serum BDNF, independent of stress or ES-CIT treatment. In conclusion, BDNF and NGF show substantial changes in this rodent model of chronic social stress, which is susceptible to antidepressant treatment with ES-CIT and therefore may constitute a neurobiological correlate for the disease. © 2009 Wiley-Liss, Inc. [source] Relationship between non-functional masticatory activity and central dopamine in stressed ratsJOURNAL OF ORAL REHABILITATION, Issue 11 2010F. M. GÓMEZ Summary, In humans, diurnal tooth-clenching and other oral stereotyped behaviour are associated with stress/anxiety. In rodents, gnawing/biting of objects is observed during exposure to stress. Both nigrostriatal and mesocortical dopaminergic systems are involved in the development of this coping behaviour. To clarify the relationship between central dopaminergic activity and stress-induced parafunctional masticatory behaviour, using microdialysis in vivo, we assessed the changes in extracellular dopamine concentrations in both prefrontal cortex and striatum of rats subjected to a mild tail pinch. The animals were divided into two groups according to the degree of non-functional masticatory activity (NFMA) displayed during exposure to tail pinch. In prefrontal cortex, rats which displayed severe NFMA showed a greater increase in extracellular dopamine concentration in relation to basal values (Emax = 184 ± 26%) than those which did not display this coping behaviour (Emax = 139 ± 23%) (FNFMA[1,86] = 3·97; P < 0·05) (n = 17). A positive association was also found between cortical dopamine maximal value from baseline and the degree of NFMA displayed (r = 0·36; P < 0·05) (n = 17). There were no significant differences in the tail-pinch-induced striatal dopamine increase between both groups of rats (Emax = 130 ± 10%) (n = 17). These results provide further evidence in support of prefrontal dopamine playing a relevant role in the expression of stress-induced masticatory coping behaviour. [source] Effects of repeated maprotiline and fluoxetine treatment on gene expression of catecholamine synthesizing enzymes in adrenal medulla of unstressed and stressed ratsAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 4 2010N. Spasojevic Summary 1,Repeated maprotiline (a noradrenaline reuptake inhibitor) and fluoxetine (a serotonin reuptake inhibitor) treatment on gene expression of catecholamine biosynthetic enzymes were examined in adrenal medulla of unstressed control and chronic unpredictable mild stressed rats. 2,Maprotiline did not change gene expression of catecholamine biosynthetic enzymes in control and stressed rats. 3,Fluoxetine increased gene expression of tyrosine hydroxylase (TH) and dopamine-,-hydroxylase (DBH), but did not phenylethanolamine N -methyltransferase in both unstressed and chronic unpredictable mild stressed animals. 4,In conclusion, we have demonstrated that repeated administration of fluoxetine enhanced gene transcription of TH and DBH and subsequently stimulates noradrenaline synthesis in adrenal medulla of control and stressed rats. [source] | ||||||||||