This study compares cortisol concentrations in plasma and milk over a time-span of 1-4h following injection of an adrenocorticotropic hormone (ACTH) or a physiological stressor. Its aim was to characterize the usefulness of milk cortisol concentrations as short-term measures of acute stress.

Experiment 1: three groups of lactating cows (Groups B - D; n = 5, each) were injected with ACTH1-24 at 4, 2 and 1h before milking, respectively, so that each experienced a similar period of elevated adrenocortical activity, but presented at milking with varying plasma cortisol concentrations. Another group (Group A; n = 5) was a saline-treated control. Mean plasma cortisol concentrations at milking were 7, 8, 24 and 56ng ml−1 for Groups A, B, C and D, respectively. Mean cortisol concentrations in milk were similar for Groups A and B (1.2 and 0.5 ng ml−1, respectively), higher in Group C (2.4ng ml−1), and greatest in Group D (11.7 ng ml−1; p <0.001).

Experiment 2: lactating dairy cows (n = 15) were injected with ACTH, transported by truck, or blood-sampled only (control) during the 2h before milking. Mean plasma cortisol concentrations at milking were 6, 20 and 72 ng ml−1 following control, ACTH and transport treatments, respectively; mean concentrations of cortisol in milk displayed a similar pattern (1.1, 2.4 and 12.0 ng ml−1, respectively; p <0.001).

Milk cortisol concentrations were highly correlated with plasma levels at milking, but did not reflect those situations where, following a period of elevation within the previous 4h, plasma cortisol concentrations had returned to basal levels. Concentrations of cortisol in foremilk and composite milk were highly correlated, but the mechanisms of cortisol flux may differ between these two compartments. Milk cortisol concentration can be a useful indicator of responses of lactating cows to acute stressors which act up to 2h before collection of samples.

Previous research has shown that pre-parturient primiparous pigs (gilts) housed in behaviourally restrictive farrowing crates without straw redirect their nest-building behaviour to non-manipulable substrates such as the bars of the crate. These gilts also show elevated plasma adrenocorticotropic hormone (ACTH) and Cortisol levels, particularly around the peak of nest-building activity, when compared to gilts in larger pens that have been provided with a manipulable substrate (straw). It remains unclear whether these behavioural and physiological responses to crating result from the lack of a suitable nesting substrate or from the restricted space. This study investigated the effects of space (crate [C] versus pen [P] and straw (straw [S] versus no straw [NS]) using a 2 × 2 factorial design. Thirty-four gilts were implanted with an indwelling jugular catheter at around 12 days before parturition. They were moved to one of the four environments five days before parturition, and blood sampling and recording of behaviour were carried out during the pre-parturient period. Penned gilts (P), irrespective of straw availability, spent more time standing and walking and performed more total substrate-directed behaviour than crated (C) gilts. When straw was not available to penned gilts, a large proportion of their substrate-directed behaviour was redirected to the floor. Space also had an effect on ACTH and Cortisol levels across the entire pre-parturient phase, with C gilts having higher levels than P gilts irrespective of straw availability, but particularly so at the peak of nest-building activity. There was no effect of straw on ACTH or Cortisol levels. Overall, it appears that increased space, perhaps through allowing locomotion, increases substrate-directed behaviour of pre-parturient gilts. When space is available but straw is absent, pre-parturient gilts redirect their nest-building behaviour to the floor. The ability to express substrate-directed behaviour as a result of increased space is reflected in lower levels of indicators of physiological stress.

In this study, we characterized secretory granules in somatotroph (STCs) and corticotroph (CTCs) cells from the anterior pituitary of rats, in conjunction with different experimental treatments with bee venom (BV). In the rats injected for 30 days with daily BV doses equivalent to one sting, we found significant changes in secretory granules' diameter: reduced by 48.15% in STCs and increased by 5.09% in CTCs, and especially a shift to gray into their intensity profile: increased by 237.04% in STCs and by 212.38% in CTCs. In the rats injected with a single high BV dose, the granules' diameter was reduced in both STCs (by 7.14%) and CTCs (by 4.67%—significant) and their gray intensity profile increased by 200% in STCs and by 51.71% in CTCs (both are significant). The changes in the gray profile reflected a reduced content of granules in the cells, consistent with an increase of the plasma levels of GH and ACTH in all cases. We concluded that the reduced hormone cargo of granules in STCs and CTCs resulted from an accelerated cell secretion. The results obtained for the two types of cells correlated, indicating a similar reaction of these secretory cells to the prolonged and acute presence of BV in the organism.

In this review article four neuropeptides: adrenocorticotrope hormone (ACTH), corticotrope releasing hormone (CRH), neuropeptide- Y(NPY) and cholecystokinin (CCK) are discussed with respect to their possible role in the pathogenesis of anxiety disorders. First the presumable working mechanism of these peptides in the brain is mentioned. In addition, the relationship of these peptides and anxiety is outlined using neuroanatomical and electrophysiological research data. Subsequently, animal experiments and human research findings are discussed. Most of the research findings so far are obtained from animal data. Only with respect to CCK, there is increasing evidence, also from human studies, that this peptide might play a role in the pathogenesis of anxiety disorders. The putative role of the other peptides remains to be estab lished in future research.

Recent findings have identified an endogenous brain system mediating the actions of cannabis sativa preparations. This system includes the brain cannabinoid receptor (CB-1) and its endogenous ligands anandamide and 2-arachidonoyl-glycerol. The endogenous cannabinoid system is not only present in the adult brain, but is also active at early stages of brain development. Studies developed at our laboratory have revealed that maternal exposure to psychoactive cannabinoid results in neuro-developmental alterations. A model is proposed in which early Δ9-tetrahydrocannabinol (THC) exposure during critical developmental periods results in permanent alterations in brain function by either the stimulation of CB-1 receptors present during the development, or by the alterations in maternal glucocorticoid secretion. Those alterations will be revealed in adulthood after challenges either with drugs (i.e. opiates) or with environmental stressors (i.e. novelty). They will include a modified pattern of neuro-chemical, endocrine, and behavioral responses that might lead ultimately to inadaptation and vulnerability to opiate abuse.

Poor maternal nutrition during pregnancy can result in increased disease risk in adult offspring. Many of these effects are proposed to be mediated via altered hypothalamo–pituitary–adrenal axis (HPAA) function, and are sex and age specific. Maternal undernutrition around the time of conception alters HPAA function in foetal and early postnatal life, but there are limited conflicting data about later effects. The aim of this study was to investigate the effect of moderate periconceptional undernutrition on HPAA function of offspring of both sexes longitudinally, from juvenile to adult life. Ewes were undernourished from 61 days before until 30 days after conception or fed ad libitum. HPAA function in offspring was assessed by arginine vasopressin plus corticotropin-releasing hormone challenge at 4, 10 and 18 months. Plasma cortisol response was lower in males than in females, and was not different between singles and twins. Periconceptional undernutrition suppressed offspring plasma cortisol but not adrenocorticotropic hormone responses. In males, this suppression was apparent by 4 months, and was more profound by 10 months, with no further change by 18 months. In females, suppression was first observed at 10 months and became more profound by 18 months. Maternal undernutrition limited to the periconceptional period has a prolonged, sex-dependent effect on adrenal function in the offspring.

The study was designed in order to gain a better understanding of whether the lack of competition stress and/or sampling time had an influence on circulating β-endorphin, adrenocorticotrophin (ACTH) and cortisol modifications after experimental showjumping sessions and to study the effects of fence height on hormone changes. Hormone levels were recorded before exercise in basal conditions and after warm-up, then 5 and 30 min post-exercise. Using a randomized crossover study design, six horses were studied during three experimental showjumping sessions over fences of different heights: 1.00 m (session 1), 1.10 m (session 2) and 1.20 m (session 3). The showjumping exercise did not modify plasma β-endorphin and serum ACTH concentrations after session 1, and tended only to maintain higher values than basal after both session 2 and session 3. The interaction fence height/time was not statistically significant for either β-endorphin or ACTH changes. Sampling time significantly affected both β-endorphin (F = 2.88; P < 0.04) and ACTH (F = 3.84; P < 0.01) changes. Serum cortisol levels were always higher than basal 5 min post-exercise, with levels falling at 30 min. The interaction fence height/time was not statistically significant, while sampling time significantly affected the results (F = 7.96; P < 0.0002). This study demonstrated no significant effects of fence height on β-endorphin, ACTH and cortisol changes. The sampling times adopted affected post-exercise changes in plasma β-endorphin, ACTH and cortisol and could have masked the effects of fence height on hormone modifications.

The aim of the study was to evaluate the association between post-traumatic disorder (PTSD) and hypothalamic–pituitary–adrenal (HPA) axis responses to the triggering trauma. A companion paper evaluates the adrenergic response and interactions between the two. We measured plasma and saliva cortisol, hourly urinary excretion of cortisol, plasma levels of adrenocorticotropin (ACTH), and the leukocyte glucocorticoid receptor (GR) density of 155 non-injured survivors of traumatic events (91 males and 64 females; 125 road traffic accidents, 19 terrorist attacks, 11 others). Measurements were taken during survivors' admissions to an emergency room (ER) of a general hospital, and in the mornings, 10 d, 1 month, and 5 months later. Symptoms of peri-traumatic dissociation, PTSD, and depression were assessed on each follow-up session. The clinician-administered PTSD scale (CAPS) conferred a diagnosis of PTSD at 5 months. Survivors with (n=31) and without (n=124) PTSD at 5 months had similar levels of hormones at all times. Plasma cortisol levels decreased with time in both groups. Female subjects had lower ACTH levels than males. PTSD in females was associated with higher levels of ACTH. In unselected cohorts of trauma survivors, PTSD is not preceded by a detectable abnormality of peripheral HPA axis hormones.

The hypothalamic–pituitary–adrenal axis (HPA axis) plays a critical role in stress management. Involvement of this physiological axis in the underlying mechanisms of panic disorder (PD) has been suggested. Studies using 35% CO2 inhalation to provoke panic found no evidence for robust increases in cortisol levels in PD. However, cortisol levels alone may not be conclusive, as this hormone is merely the end product of a complex physiological axis. Sixteen PD patients and 16 healthy control subjects underwent a 35% CO2 inhalation and a placebo inhalation on separate days according to a fixed order, double-blind design. Both serum and salivary cortisol, as well as adrenocorticotropic hormone (ACTH) were measured at regular time intervals. Cortisol and ACTH levels increased in the patient and control groups following 35% CO2 inhalation. The magnitude of the increase was similar in patients and controls despite marked differences in anxiety. This study is the first to document a clear HPA response following 35% CO2 inhalation in both PD patients and controls. This effect occurs independently of the specific panicogenic properties of the CO2 challenge. It remains to be clarified whether panic is initially accompanied by major HPA axis activation or whether other stress-responsive systems underlie panic.

Plasma cortisol concentrations were determined from the blood of eight mature female reindeer (Rangifer tarandus tarandus) after an intravenous injection of either saline (control) or 100, 250 or 500 μg of synthetic ACTH. Blood samples were collected at 0, 2, 4, 6, 8, 10, 15, 20, 25, 30, 45, 60, 75, 90, 120, 150, and 180 min after the injections. The aims were to determine the appropriate dose of ACTH for adrenal stimulation tests, to define the dose level of ACTH which elicited a maximal cortisol response and to describe the range of blood cortisol concentrations for reference when evaluating the stress responses of reindeer.

The mean plasma cortisol concentrations (s.e.) at the zero sample times (t0) of the control and the ACTH treatments varied between 93·4 (11·8) and 132·5 (18·1) nmol/l. The total plasma cortisol response (area under curve, AUC, nmol/l × min) increased with increasing dose of ACTH (P < 0·001). The AUC of the control treatment was significantly smaller than of the ACTH treatments (P < 0·001). The highest dose of ACTH (500 μg) gave a significantly bigger AUC than the lowest dose (100 μg) (P = 0·008). The maximal plasma cortisol concentrations (CMAX) were achieved within 60 min of the ACTH injections. The ranges of individual CMAX were 59·0 to 136·8 nmol/l for the control treatment, and 110·0 to 252·0, 152·0 to 247·5 and 135·1 to 257·1 nmol/l for 100, 250 and 500 μg ACTH, respectively. The difference in CMAX was significant between the control treatment and the ACTH treatments (P < 0·001) but not between the different doses of ACTH. The plasma cortisol concentrations at the end of the observation period at t180 were not significantly affected by the ACTH treatment (P > 0·05).

In conclusion, the 100-μg dose of ACTH was sufficient to produce a significant cortisol response compared with the control treatment. Increasing the dose did not increase the maximal response, but tended to elongate the response profile. The blood sampling frequency used in the study was found suitable for detection of the cortisol response in reindeer.

Baseline ACTH values were assessed in a large sample of depressed patients to establish correlations with baseline and post-dexamethasone cortisol levels. No statistically significant differences were found, indicating that excessive ACTH release mighl not be responsible for the elevated cortisol levels and nonsuppression by dexamethasone frequently observed in these patients. Other extrahypophyseal factors may mediate these responses.