Differential effects of forced swim-stress on the corticotropin-releasing hormone and vasopressin gene transcription in the parvocellular division of the paraventricular nucleus of rat hypothalamus

Role of the basolateral amygdala in mediating the effects of the fatty acid amide hydrolase inhibitor URB597 on HPA axis response to stress

“…Our results also confirm a previous report showing that 10 min of forced swimming increases CRH heteronuclear RNA (hnRNA) in PVN, which returns to basal levels within 2 h (Jiang et al, 2004). As expected, the increase of CRH mRNA in PVN was accompanied by increased POMC mRNA levels in the pituitary gland, as already well documented by previous studies (Jiang et al, 2004).…”

Effect of Various Physical Stress Models on Serum Cortisol Level in Wistar Rats

“…As shown in [Table/ Fig-1] serum cortisol levels were significantly higher after forced swim test in male rats. Similar results were observed by Jiang Ya-Q et al, [9] and Preeti Kothiyal et al, [10] They observed that glucocorticoid levels were increased when rats were subjected to forced swim test till complete exhaustion. They concluded that stress in optimum quantum acted as stimulator to achieve the best, but when it exceeded, it caused imbalance in biochemical parameters as well as it lead to suppression in physical endurance.…”

The effects of CRF antagonists, antalarmin, CP154,526, LWH234, and R121919, in the forced swim test and on swim-induced increases in adrenocorticotropin in rats

“…It is interesting to note that none of the CRF antagonists completely blocked swim-induced increases in ACTH, such that ACTH levels never returned to baseline values after CRF antagonist treatment. Similarly, a previous study demonstrated that the synthetic glucocorticoid, dexamethasone, failed to completely suppress swim-stress-induced ACTH increases (Jiang et al 2004). These findings suggest that other factors or stress-related neuropeptides may be continuing to increase ACTH during swimming.…”

“…The release of these peptides was reported to be differently regulated by different stressors (Plotsky 1987). Likewise, forced swim stress differentially altered CRF and AVP transcription (Jiang et al 2004), and the ACTH response in AVP-deficient rats as compared to control rats was not altered by hypertonic saline stress, but was diminished after the 10-min swim stress (Makara et al 2004). Interestingly, vasopressin was proposed as a potential target of antidepressant therapy, and vasopressin antagonists were shown to have antidepressant activity in preclinical models (for review, see Scott and Dinan, 2002;Griebel et al 2002a,b;Alonso et al 2004).…”