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
Li Li, Xiaohua Li, Wenjun Zhou and Joseph L Messina
M. S. Harbuz and S. L. Lightman
In-situ hybridization histochemistry was used to measure corticotrophin-releasing factor mRNA and proenkephalin A mRNA in the paraventricular nucleus (PVN), and pro-opiomelanocortin (POMC) mRNA in the anterior pituitary of the rat. Levels of message were determined at 1, 2, 4 and 8 h after exposure to a variety of physical and psychological stresses. Corticotrophin-releasing factor mRNA in the PVN and POMC mRNA in the anterior pituitary increased in response to i.p. hypertonic saline, restraint and swim stress but not to cold stress. Proenkephalin A mRNA was raised only in response to the physical stress of i.p. injection of hypertonic saline. These results suggest that different afferent pathways and hypothalamic neurotransmitters may be involved in mediating the hypothalamic response to different physical and psychological stresses.
Journal of Endocrinology (1989) 122, 705–711
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
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
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
R. F. Parrott, S. N. Thornton, M. L. Forsling and C. E. Delaney
The effect of stress on drinking, water balance and endocrine profile was studied using ten castrated rams. Individual sheep were exposed to 30-h periods of total isolation (psychological stress) or physical separation from their social group (control). Plasma was analysed for haematocrit, osmolality, electrolyte levels and concentrations of cortisol and arginine vasopressin. Isolation stress significantly reduced water intake, increased haematocrit and plasma concentration of cortisol, but did not alter osmolality or vasopressin concentration. The physiological effects of this self-imposed water restriction contrast with those obtained by depriving the sheep of water for 24 h under conditions that were not stressful, i.e. by keeping them grouped together. These results suggest that cortisol may act to defend plasma volume in sheep exposed to acute stress. The results also indicate that vasopressin probably should not be considered to be a 'stress hormone' in the sheep.
J. Endocr. (1987) 112, 305–310
An ultrastructural study is described which relates cellular activity in the intermediate lobe of the pituitary gland with circulating levels of corticosterone. Exposure of male CSF rats to a signalled, unpredictable 60-day stress regimen induced intense secretory activity in all cells of the pars intermedia for the first 5 days of stressing, and thereafter secretory activity reverted back to the control condition. Blood corticosterone levels showed an initial extreme increase lasting for the first 5 days of exposure to the stress before gradually falling to re-establish a new stable level of secretion by 40 days. The possible involvement of the intermediate lobe in emotional or psychological stress when corticosterone levels are high is discussed.
P. W. P. BUTLER, G. M. BESSER and HANNAH STEINBERG
A close relationship exists between the activity of the pituitary—adrenal system and the psychological state of a subject. For example, marked mood changes occur in Cushing's syndrome and in Addison's disease (Michael & Gibbons, 1963) and severe depression may increase the plasma cortisol concentration and abolish its physiological diurnal rhythm (Gibbons & McHugh, 1962; Besser & Butler, 1967). Other forms of stress such as surgical operations (Estep, Island, Ney & Liddle, 1963) have similar effects as does hypoglycaemia (Landon, Wynn & James, 1963). We now report the effect on the plasma cortisol level in man of two centrally acting drugs: dexamphetamine, which has predominantly stimulant actions, and chlordiazepoxide, a benzodiazepine which is now much used in the treatment of anxiety instead of small doses of barbiturates. The drugs were given separately and in combination.
Forty-four healthy volunteers (aged 18–32, 32 male) were randomly divided into four equal groups. All subjects
M. T. JONES and P. K. BRIDGES
In earlier studies (Bridges & Jones, 1967, 1968) we found a significant relationship between adrenocortical responses to the psychological stress of an oral university examination (2nd M.B. Anatomy examination) and body-build, assessed by means of phenotyping by the method of Parnell (1958). This assumes three basic components of physique: fatness (F), muscularity (M) and linearity (L). It was found that the mean plasma corticosteroid concentration at the time of the examination was significantly greater in the primarily linear group than in the mainly muscular students, and there was a significant negative correlation between the examination corticosteroid values and the muscularity scores (r = − 0·225; P < 0·05). One explanation for these findings would be that the muscular group was characterized by a lower sensitivity of adrenocortical response. It was decided to test this possibility using the methods of Landon, James, Wharton & Friedman (1967).
For the present study, 38 students
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.