Stress, hormone response

In addition to the classical stress hormones already reviewed, several other hormones are augmented in response to stress. Stress-induced prolactin release is one of the most frequently studied examples. There is no doubt about the causal relationship between stress and increased pituitary prolactin release, but the biological meaning is much less clear (G2). This phylogenetically old hormone has been shown to have more than 85 different functions in all vertebrate species. However, besides its role in the induction of maternal lactogenesis, the physiological importance of prolactin is at present not fully established. Experimental and clinical evidence supports the view that prolactin is also an immunoregulating hormone (M44, R18). Prolactin receptors are present on human T and B lymphocytes (R18), and T lymphocytes depend on prolactin for maintenance of immunocompetence (B19). In addition, it has been shown that prolactin is able to influence the devel-... 

Stressful early life events, involving abuse or neglect, can have a life-long influence on the stress response, and lead to elevated levels of allostatic load for the lifespan. Overactivity of the stress hormone axis has been linked to prenatal stress or poor maternal care in rodent models, and this overactivity contributes to increased rates of brain and body aging [39]. 

The impacts of contaminants on the structure of the immune system can be assessed by examining white blood cell (WBC) numbers and the mass and cellularity of immune organs, although these indicators are usually not as sensitive as measures of immune function. Avian immunotoxicity studies frequently assess total and (or) differential WBC counts [79], and immunosuppression can be indicated by reduced numbers of WBCs or elevated WBC numbers caused by recurrent infections. An elevated heterophil to lymphocyte ratio can indicate altered immune status in response to corticosteroid stress hormones or other factors [78,7 9], Exposure to lead shot or lead acetate has been shown to alter total and (or) differential WBC numbers in Japanese quail (Coturnix coturnix) and mallards [81-83], In western grebes (Aechmophorus occidentalis) from California, concentrations of mercury in the kidney were positively correlated with heterophil... 

Moore, I.T., LeMaster, M.P. and Mason, R.T. (2000) Behavioural and hormonal responses to capture stress in the male red-sided garter snake, Thamnophis sirtalis parietalis. Anim. Behav. 59, 529-534. 

In relatively recent years, it has become clear that under-nntrition of mother leads to low birth weight of the baby and this can increase the risk of development of degenerative disease in later life, e.g. hypertension, obesity, type 2 diabetes. One hypothesis is that the foetus adapts meta-bolically to deficiencies by increasing the number of cells in organs that perform specific functions that can overcome the deficiency, e.g. an increase in the number of liver cells that carry out gluconeogenesis, an increase in cells in the adrenal cortex to produce more of the chronic stress hormone, cortisol. These changes are carried over into adnlthood which can lead to an inadequate response of the liver to insulin so that insulin resistance develops. So far, however, it is unclear whether deficiencies in specific nntrients or undemutrition per se are responsible for snch changes (Chapter 15). 

GC, in turn, exert a very sensitive negative feedback on the HPA system at the level of the paraventricular nucleus of the hypothalamus (PVN) and the anterior pituitary, and also at the level of the hippocampus, which projects to the bed nucleus of the stria terminalis, the latter which sends off projections to the PVN. In concert with other components of the stress hormone system, the action of corticosterone displays two modes of operation (for review see De Kloet et al. 1998). In the first proactive mode, GC maintain basal activity of the HPA system and control the sensitivity or threshold of the system s response to stress. GC promote coordination of circadian events, such as the... 

Few studies have examined noradrenergic function in patients with phobic disorders. In patients with specific phobias, increases in subjective anxiety and increased heart rate, blood pressure, plasma NE, and epinephrine have been associated with exposure to the phobic stimulus (Nesse et al. 1985). This finding may be of interest from the standpoint of the model of conditioned fear, reviewed above, in which a potentiated release of NE occurs in response to a reexposure to the original stressful stimulus. Patients with social phobia have been found to have greater increases in plasma NE in comparison to healthy controls and patients with panic disorder (Stein et al. 1992). In contrast to panic disorder patients, the density of lymphocyte a-adrenoceptors is normal in social phobic patients (Stein et al. 1993). The growth hormone response to intravenous clonidine (a marker of central a2-receptor function) is blunted in social phobia patients (Tancer et al. 1990). 

Although it is estimated that 61% of men and 51% of women experience at least one serious traumatic event during their lifetime, the incidence of PTSD in the general population is only about 7%. This suggests that certain people are particularly vulnerable and that there may be a preexisting condition that leads someone to develop PTSD. Indeed, much of the current research under way on PTSD is focused on individual differences in factors such as the hormonal response to stress that may incline someone toward acquiring this illness. 

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