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Li Li, Xiaohua Li, Wenjun Zhou and Joseph L Messina

kinase ( Pessin & Saltiel 2000 , Saltiel & Kahn 2001 ). There are multiple proposed pathophysiological mechanisms for the association between chronic psychological stress or depression and insulin resistance or diabetes ( Lewis et al . 1983 , Winokur

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Chad D Osterlund, Vanessa Thompson, Laura Hinds and Robert L Spencer

essential intracellular signaling proteins for virtually all cell types, including neurons and endocrine cells ( Grewal et al . 1999 ). We recently have reported that acute exposure to psychological stress (restraint) increased the activated (phosphorylated

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Elin Kristensson, Monika Sundqvist, Rolf Håkanson and Erik Lindström

raised in response to psychological stress in both SPD rats and WKY rats ( Kristensson et al. 2006 ), and that ghrelin expression in the oxyntic mucosa is increased in response to stressful stimuli such as tail pinch ( Asakawa et al. 2001 ) and

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Tsukasa Nozu, Saori Miyagishi, Rintaro Nozu, Kaoru Takakusaki and Toshikatsu Okumura

, the roles were also evaluated on these altered visceral changes induced by LPS (immune stress) or repeated WAS (psychological stress), which are considered to be experimental animal models of IBS ( Larauche et al. 2012 , Nozu et al. 2017 a , b

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TL Coventry, DS Jessop, DP Finn, MD Crabb, H Kinoshita and MS Harbuz

Endomorphin (EM)-1 and EM-2 are opioid tetrapeptides recently located in the central nervous system and immune tissues with high selectivity and affinity for the mu-opioid receptor. Intracerebroventricular (i.c.v.) administration of morphine stimulates the hypothalamo-pituitary-adrenal (HPA) axis. The present study investigated the effect of centrally administered EM-1 and EM-2 on HPA axis activation. Rats received a single i.c.v. injection of either EM-1 (0.1, 1.0, 10 microg), EM-2 (10 microg), morphine (10 microg), or vehicle (0.9% saline). Blood samples for plasma corticosterone determinations were taken immediately prior to i.c.v. administration and at various time points up to 4 h post-injection. Trunk blood, brains and pituitaries were collected at 4 h. Intracerebroventricular morphine increased plasma corticosterone levels within 30 min, whereas EM-1 and EM-2 were without effect. In addition, pre-treatment of i.c.v. EM-1 did not block the rise in corticosterone after morphine. Corticotrophin-releasing factor (CRF) mRNA and arginine vasopressin (AVP) mRNA in the paraventricular nucleus (PVN) and POMC mRNA in the anterior pituitary were found to be unaffected by either morphine or endomorphins. Since release of other opioids are elevated in response to acute stress, we exposed rats to a range of stressors to determine whether plasma EM-1 and EM-2 can be stimulated by HPA axis activation. Plasma corticosterone, ACTH and beta-endorphin were elevated following acute restraint stress, but concentrations of plasma EM-1-immunoreactivity (ir) and EM-2-ir did not change significantly. Corticosterone, ACTH and beta-endorphin were further elevated in adjuvant-induced arthritis (AA) rats by a single injection of lipopolysaccharide (LPS), but not by restraint stress. In conclusion, neither EM-1 or EM-2 appear to influence the regulation of the HPA axis. These data suggest that endomorphins may be acting on a different subset of the mu-opioid receptor than morphine. The failure to induce changes in plasma EM-ir in response to the chronic inflammatory stress of AA, the acute immunological stress of LPS, or the psychological stress of restraint, argues against an important role for endomorphins in mediating HPA axis activity.

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Keiko Nakahara, Rieko Okame, Tetsuro Katayama, Mikiya Miyazato, Kenji Kangawa and Noboru Murakami

responses. Plasma ghrelin levels decreased significantly from 20 min onward during stress treatments. On the other hand, acute psychological stress raises them ( Kristenssson et al . 2006 ). In addition, Zimmermann et al . (2007) have reported that

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George Fink

conclusion that stress, but not H. pylori , is associated with peptic ulcer disease in this Thai population ( Wachirawat et al. 2003 ). Finally, a recent population-based Danish cohort ( n  = 2410) study showed that psychological stress increased the

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Menghong Yan and Qiwei Zhai

). Likewise, the offspring whose fathers experienced psychological stress show elevated blood glucose and increased hepatic gluconeogenesis ( Wu et al. 2016 ). These findings demonstrate that paternal stress may lead to metabolic disorders in offspring

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S Hesketh, D S Jessop, S Hogg and M S Harbuz

within the pPVN, that may have a role in the mediation of the stress response ( Neumann et al. 2000 a , b , Nakashima et al. 2002 , Neumann 2002 ). Restraint stress is a well documented predominantly psychological stressor ( Pare & Glavin

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Saadia Basharat, Jennifer A Parker, Kevin G Murphy, Stephen R Bloom, Julia C Buckingham and Christopher D John

psychological stress ( Connor & Leonard 1998 ), ultimately activate the HPA axis via a convergence at the hypothalamus to precipitate the CRH–ACTH–glucocorticoid cascade, there is surprisingly little overlap in the sets of genes within the brain that are induced