Acute assessment of subjective appetite and implicated hormones after a hypnosis-induced hallucinated meal: a randomized cross-over pilot trial.

The use of hypnosis can generate hallucinatory phenomena, which ranged from vivid/auditory imagery to fully developed "hallucinations" in selected people. The aim of this pilot trial was investigating the acute effects of a hypnosis-induced hallucinated breakfast (HB) compared to those of a real breakfast (RB) on subjective appetite and appetite-regulating hormones in highly hypnotizable individuals. Eight healthy post-menopausal women were recruited to consume two meals: the HB and the RB in a randomized crossover design. Participants underwent appetite sensations measurements (before meal and each 30-min until 270-min) and blood sample collection (at 0, 20, 60, 90, 180-min). A 3-day food-record was filled after each meal. The adjusted repeated measures ANCOVA did not show any meal×time interactions on subjective appetite postprandially. As expected, significantly higher glucose (p < 0.001), insulin (p < 0.001), and lower free fatty acid (p < 0.001) concentrations were found after the RB, but not following HB. Furthermore, RB significantly increased postprandial levels of glucagon-like-peptide-1 and peptide-YY at 20, 60, 90 and 180-min, whereas acylated-ghrelin and leptin levels did not differ. Postprandial neuropeptide-Y and orexin-A values significantly increased at different time-points after RB, but not following HB, while α-melanocyte-stimulating hormone levels enhanced after HB only. Energy intakes were significantly lower after HB on the test-day only (HB = 1146.6 ± 343.8 vs RB = 1634.7 ± 274.2 kcal/d; p = 0.003). Appetite sensation might be modulated by fully developed meal "hallucination" induced by hypnosis, likely affecting brain-peptides implicated in the appetite regulation. However, further studies are needed to verify these results obtained in a highly selected group of individuals. NCT03934580.

Paternal hyperglycemia in rats exacerbates the development of obesity in offspring.

Parental history with obesity or diabetes will increase the risk for developing metabolic diseases in offspring. However, literatures as to transgenerational inheritance of metabolic dysfunctions through male lineage are relatively scarce. In the current study, we aimed to evaluate influences of paternal hyperglycemia on metabolic phenotypes in offspring. Male SD rats were i.p. injected with streptozotocin (STZ) or citrate buffer (CB, as control). STZ-injected rats with glucose levels higher than 16.7 mM were selected to breed with normal female rats. Offspring from STZ or CB treated fathers (STZ-O and CB-O) were maintained in the identical condition. We monitored body weight and food intake, and tests of glucose and insulin tolerance (GTTs and ITTs), fasting-refeeding and cold exposure were performed. Expression of factors involved in hypothalamic feeding and brown adipose tissue (BAT) thermogenic activity was performed by real-time PCR and Western blot. Adult STZ-O were heavier than CB-O. Impairment of GTTs was observed in STZ-O compared with CB-O at 22 and 32 weeks of age; ITTs results showed decreased insulin sensitivity in STZ-O. Daily food intake and accumulated food intake during 12-h refeeding after fasting were significantly higher in STZ-O. UCP1 levels were downregulated in BAT from STZ-O at room temperature and cold exposure. Finally, STZ-O rats showed suppressed leptin signaling in the hypothalamus as evidenced by upregulated SOCS3, reduced phosphorylation of STAT3, impaired processing POMC and decreased α-MSH production. Our study revealed that paternal hyperglycemia predisposes offspring to developing obesity, which is possibly associated with impaired hypothalamic leptin signaling.

The Preventive Effect of Coffee Compounds on Dermatitis and Epidermal Pigmentation after Ultraviolet Irradiation in Mice.

BACKGROUND: Ultraviolet (UV) irradiation is well known to promote inflammation and pigmentation of skin. UVB mainly affects dermatitis and pigmentation. Coffee contains a number of polyphenols, such as caffeic acid (CA) and chlorogenic acid (CGA) but their in vivo bioactivity for photobiology remains unclear. METHODS: C57BL/6j male mice were irradiated with UVB (1.0 kJ/m2/day) for 3 days. Five days after the final session of UVB irradiation, the dorsal skin, ear epidermis, and blood samples were analyzed to investigate the inflammatory factors, melanogenesis factors and related hormones. RESULTS: After the oral administration of CA (100 mg/day) or CGA (100 mg/day) for 8 days, only CA was found to inhibit dermatitis and pigmentation. The pathway by which CA inhibits dermatitis is related to the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK)1/2/cAMP response element binding protein (CREB) pathway. Otherwise, the pathway by which CA inhibits pigmentation is related to the activation of the ß-endorphin-µ-opioid receptor and suppresses the cAMP-microphthalmia-associated transcription factor (MITF) pathway. CONCLUSION: It is suggested that the oral administration of CA prevented dermatitis and pigmentation after UVB irradiation in mice.

Weight gain in risperidone therapy: investigation of peripheral hypothalamic neurohormone levels in psychotic patients.

The use of antipsychotic drugs has started a new era in the treatment of psychotic disorders. Nevertheless, they cause complications in the long-term treatment, which is mainly weight gain. In this study, we investigated circulating levels of hypothalamic neuropeptides, which are related to appetite regulation, neuropeptide Y (NPY), α-melanocyte-stimulating hormone (α-MSH), cocaine- and amphetamine-regulated transcript (CART), and leptin, in first-attack psychotic patients who were treated with an atypical antipsychotic drug, risperidone, for 4 weeks. We used a case-control association design to compare the neuropeptides in the control group versus before and after treatment of the patient group. Samples were obtained from psychotic patients who were admitted to the Psychiatry Outpatient Clinics, Gulhane School of Medicine, Ankara, Turkey. When compared with the control group, NPY and α-MSH plasma levels of psychotic patients were severely reduced, and the CART levels were substantially increased when they were first diagnosed (before treatment). However, the patients' body mass index and circulating leptin levels were markedly high after the treatment. Circulating levels of those neurohormones were not significantly changed between before and after treatment of the patients. These data demonstrate that peripheral α-MSH and NPY, although reflecting only secretion from peripheral organs, nevertheless, may provide an insight into the patients sympathetic tone and also suggest change of their appetite regulation. α-Melanocyte-stimulating hormone, NPY, and CART plasma levels may be used as a predictor of weight gain in the early treatment of the patients along with the leptin levels.

The investigation of leptin and hypothalamic neuropeptides role in first attack psychotic male patients: olanzapine monotherapy.

The mechanism underlying the weight gain due to treatment with olanzapine and other second generation antipsychotics has not been fully understood. To examine olanzapine's weight gain effects, we accepted first attack psychotic patients with no medication (pre-treatment) (n=22) and the healthy control group (n=26) in this study. After patients diagnosis, they were hospitalized and then treated for four weeks with olanzapine (post-treatment). We used case-control association design to test body mass index (BMI) and biochemical changes in each group. We also investigated peripheral leptin and neuropeptides/hormones namely, pro-opiomelanocortin (POMC), cocaine and amphetaime regulated transcript (CART), and neuropeptide Y (NPY) levels. These neuropeptides which are synthesized/secreted from arcuate nucleus of hypothalamus affect food intake and therefore, body weight. After 4 weeks of olanzapine treatment; BMI (body mass index), waist circumference, blood triglyceride, total cholesterol, and very low density lipoprotein (VLDL) levels were increased significantly in patients compared to their pre-treatment baseline. In pre-treatment, patients' NPY levels were significantly lower while α-MSH, the anorexigenic product of POMC levels were significantly higher vs. control. Both leptin and NPY levels were significantly increased in patients after the treatment but the NPY levels were also significantly lower in post-treatment vs. the control group. The CART levels did not change after the treatment. We may presume that the antagonist effect of olanzapine on the serotonin (5HT2CR and 5HT1BR) receptors of the arcuate hypothalamic neurons may be a basis for a deregulation of the neurohormones secretion.

Regulation of feeding and anxiety by alpha-MSH reactive autoantibodies.

alpha-Melanocyte-stimulating hormone (alpha-MSH) is a stress-related neuropeptide involved in the regulation of motivated behavior, appetite and emotion including stimulation of satiety and anxiety. Although autoantibodies (autoAbs) reactive with alpha-MSH have been identified in human subjects and in rats, it remained unknown if these autoAbs are involved in the regulation of feeding and anxiety and if their production is related to stress. Here we show that repeated exposure of rats to anxiolytic mild stress by handling increases the levels and affinity of alpha-MSH reactive IgG autoAbs and that these changes are associated with adaptive feeding and anxiety responses during exposure of rats to a strong stress by food restriction. Importantly, an increase in affinity of alpha-MSH reactive autoAbs was associated with changes of their functional roles from stimulation to inhibition of alpha-MSH-mediated behavioural responses, suggesting that these autoAbs can be a carrier or a neutralizing molecule of alpha-MSH peptide, respectively. Using a model of passive transfer into the brain, we show that alpha-MSH autoAbs affinity purified from blood of rats exposed to repeated mild stress, but not from control rats, are able to increase acutely food intake, suppress anxiety and modify gene expression of hypothalamic neuropeptides in naïve rats. These data provide the first evidence that autoAbs reactive with alpha-MSH are involved in the physiological regulation of feeding and mood, supporting a further role of the immune system in the control of motivated behavior and adaptation to stress.

The effect of age on serum antibody titers after rabies and influenza vaccination in healthy horses.

BACKGROUND: The proportion of geriatric horses within the equine population has increased in the past decade, but there is limited information on the immune function of these animals. HYPOTHESIS: Aged horses will have a lesser increase in serum antibody response to vaccination. ANIMALS: Thirty-four aged healthy horses (> or = 20 years) and 29 younger adult horses (4-12 years) of various breeds. METHODS: All horses were vaccinated with vaccines of killed rabies and influenza virus. Horses in each age group were allocated to receive either rabies or influenza booster vaccine 4 weeks after the initial vaccination. Serum samples were taken at 0, 4, 8, and 24 weeks. Rabies serum neutralization titers and equine influenza virus specific antibody sub-isotypes (IgGa, IgGb, IgG(T), and IgA) as well as single radial hemolysis (SRH) titers were determined. RESULTS: Rabies antibody titers were similar in the 2 age groups at all sampling times. Aged horses had higher IgGa and IgGb influenza antibody titers before vaccination than younger horses but similar titers after vaccination (P= .004 and P= .0027, respectively). Younger horses had significantly greater increases in titer than aged horses at all sampling times for IgGa (P= .001) and at 8 and 24 weeks for IgGb (P= .041 and .01, respectively). There was no detectable serum IgG(T) at any time point. A significant booster vaccine effect was seen for both antirabies and anti-influenza titers. Anti-influenza titer before vaccination also had a significant effect on subsequent antibody response. CONCLUSIONS AND CLINICAL IMPORTANCE: Healthy aged horses generated a primary immune response to a killed rabies vaccine similar to that of younger adult horses. Aged horses had a significantly reduced anamnestic response to influenza vaccine.

Low temperature stimulates alpha-melanophore-stimulating hormone secretion and inhibits background adaptation in Xenopus laevis.

It is well-known that alpha-melanophore-stimulating hormone (alpha-MSH) release from the amphibian pars intermedia (PI) depends on the light condition of the animal's background, permitting the animal to adapt the colour of its skin to background light intensity. In the present study, we carried out nine experiments on the effect of low temperature on this skin adaptation process in the toad Xenopus laevis, using the skin melanophore index (MI) bioassay and a radioimmunoassay to measure skin colour adaptation and alpha-MSH secretion, respectively. We show that temperatures below 8 degrees C stimulate alpha-MSH secretion and skin darkening, with a maximum at 5 degrees C, independent of the illumination state of the background. No significant stimulatory effect of low temperature on the MI and alpha-MSH plasma contents was noted when the experiment was repeated with toads from which the neurointermediate lobe (NIL) had been surgically extirpated. This indicates that low temperature stimulates alpha-MSH release from melanotrope cells located in the PI. An in vitro superfusion study with the NIL demonstrated that low temperature does not act directly on the PI. A possible role of the central nervous system in cold-induced alpha-MSH release from the PI was tested by studying the hypothalamic expression of c-Fos (as an indicator for neuronal activity) and the coexistence of c-Fos with the regulators of melanotrope cell activity, neuropeptide Y (NPY) and thyrotrophin-releasing hormone (TRH), using double fluorescence immunocytochemistry. Upon lowering temperature from 22 degrees C to 5 degrees C, in white-adapted animals c-Fos expression decreased in NPY-producing suprachiasmatic-melanotrope-inhibiting neurones (SMIN) in the ventrolateral area of the suprachiasmatic nucleus (SC) but increased in TRH-containing neurones of the magnocellular nucleus. TRH is known to stimulate melanotrope alpha-MSH release. We conclude that temperatures around 5 degrees C inactivate the SMIN in the SC and activate TRH-neurones in the magnocellular nucleus, resulting in enhanced alpha-MSH secretion from the PI, darkening the skin of white-adapted X. laevis.

Ultraviolet B irradiation of the eye activates a nitric oxide-dependent hypothalamopituitary proopiomelanocortin pathway and modulates functions of alpha-melanocyte-stimulating hormone-responsive cells.

Ultraviolet B radiation increases DOPA-positive melanocytes in the skin specifically at the site of exposure. We found unexpectedly that ultraviolet B irradiation of the eye increased the concentration of alpha-melanocyte-stimulating hormone in plasma and systemically stimulated epidermal melanocytes in mice. To test the possible involvement of hypothalamopituitary proopiomelanocortin system in the systemic activation of skin melanocytes, ultraviolet B was also irradiated to the eye after hypophysectomy. Hypophysectomy strongly inhibited the ultraviolet B-induced stimulation of melanocytes. To elucidate the pathway by which ultraviolet B irradiation of the eye activated the hypothalamopituitary system, we examined the effect of bilateral ciliary ganglionectomy and denervation of the optic nerves on the ultraviolet B-induced melanocyte stimulation. Ciliary ganglionectomy, but not optic nerve denervation, strongly inhibited melanocyte stimulation by localized irradiation of the eye. Furthermore, melanocyte stimulation by localized ultraviolet B irradiation of the eye was not observed in mice that lack the inducible type of nitric oxide synthase. These results clearly indicate that a signal evoked by ultraviolet B irradiation of the eye is transmitted in a nitric oxide-dependent manner through the ciliary ganglia involving the first branch of the trigeminal nerve to the hypothalamopituitary proopiomelanocortin system, resulting in upregulation of alpha-melanocyte-stimulating hormone secretion and consequent stimulation of melanocytes in the skin. The novel network involving the trigeminal nerve and nitric oxide-dependent signaling pathway might play important parts in the activation of proopiomelanocortin-dependent biologic reactions, such as alpha-melanocyte-stimulating hormone-induced stimulation of melanocytes in the skin, in ultraviolet B-enriched environments.

Pituitary proopiomelanocortin-derived peptides and hypothalamus-pituitary-interrenal axis activity in gilthead sea bream (Sparus aurata) during prolonged crowding stress: differential regulation of adrenocorticotropin hormone and alpha-melanocyte-stimulating hormone release by corticotropin-releasing hormone and thyrotropin-releasing hormone.

Plasma levels of cortisol, growth hormone (GH), adrenocorticotropin hormone (ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), N-acetyl-beta-endorphin, in vitro ACTH-stimulated cortisol secretion, and in vitro corticotropin-releasing hormone (CRH)- and thyrotropin-releasing hormone (TRH)-stimulated ACTH and alpha-MSH secretion were investigated in gilthead sea bream exposed to high stocking density (30 kg m(-3)) for 23 days. Within 3 days after the onset of crowding, plasma levels of cortisol, ACTH, alpha-MSH, and N-acetyl-beta-endorphin were above control values. After 7 days, plasma parameters had returned to control levels, but at 23 days, cortisol, alpha-MSH, and N-acetyl-beta-endorphin levels were again elevated over controls, indicating a long-term activation of the melanotrope cells. In contrast, crowding stress elicited a prolonged reduction in plasma GH levels concomitant with the increased hypothalamus-pituitary-interrenal axis (HPI) activation. Crowding stress enhanced cortisol secretory activity of the unstimulated interrenal cells. However, interrenal tissue from crowded fish in vitro displayed an attenuated response to ACTH stimulation compared with tissue from control fish, indicating a desensitization of these cells to ACTH during crowding. The involvement of pituitary proopiomelanocortin-derived peptides in the HPI axis of sea bream is indicated by the observed modulation of the CRH and TRH responsiveness of the corticotropes and melanotropes in crowded fish. At day 1, when there were crowding-induced plasma increases in ACTH and alpha-MSH, there was an attenuated CRH-stimulated but not TRH-stimulated, ACTH release. However, at that time, CRH- and TRH-induced responses of alpha-MSH secretion, and the unstimulated secretory activity of the MSH cells, were enhanced in crowded sea bream. These data provide evidence for stimulatory roles of multiple hypothalamic (CRH and TRH) and pituitary (ACTH and alpha-MSH) peptides in the activation of the hypothalamus-pituitary-interrenal axis under crowding conditions in sea bream.

Diurnal variation in alpha-melanocyte-stimulating hormone content of various brain regions and plasma of the Texas toad, Bufo speciosus.

We measured the concentrations of alpha-melanocyte-stimulating hormone (alpha-MSH) in various brain regions as well as in the pituitary gland and plasma of the toad Bufo speciosus during a 24-hr light:dark cycle. There was significant diurnal variation of alpha-MSH concentrations in the hypothalamus and brainstem. In both areas alpha-MSH concentrations were highest during the scotophase. Peak alpha-MSH concentrations in the hypothalamus were observed at 21.00 and 05.00 hr, while a single peak in alpha-MSH concentrations was observed in the brainstem at 21.00 hr. In contrast, peak alpha-MSH concentrations in the plasma were observed during the photophase at 17.00 hr, when brain concentrations of alpha-MSH were low. There was no significant diurnal variation observed in the pituitary content of alpha-MSH throughout the 24-hr light:dark cycle. These data suggest that different mechanisms control hypothalamic and pituitary alpha-MSH cells in the toad during the 24-hr light:dark cycle. The fact that peak alpha-MSH concentrations were observed in the hypothalamus during the activity period of the toad is consistent with the proposed role of alpha-MSH peptides in learning and memory processes.

Non-NMDA receptor-mediated regulation of hypothalamic dopaminergic neurons in the rat.

The purpose of the present study was to examine the effects of non-NMDA receptor blockade and activation on the activity of tuberoinfundibular dopaminergic (TIDA), periventricular-hypophysial dopaminergic (PHDA) and, for comparison, nigrostriatal dopaminergic (NSDA) neurons in male and female rats. The activity of TIDA, PHDA and NSDA neurons was estimated by measuring the concentration of the primary dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence, intermediate lobe of the posterior pituitary and striatum, respectively. Systemic administration of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-selective antagonist 6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3(1H,4H)-dione (NBQX) increased DOPAC concentrations in the median eminence and intermediate lobe, and decreased plasma concentrations of prolactin and alpha-MSH, in a dose- and time-related manner. In contrast, NBQX had no effect on DOPAC concentrations in the striatum, suggesting that non-NMDA receptors are not involved in the tonic regulation of NSDA neurons. The increase in DOPAC concentrations in the median eminence and intermediate lobe, and the decrease in plasma concentrations of prolactin and alpha-MSH, produced by NBQX were prevented by AMPA but not by kainic acid. Taken together, the results demonstrate that endogenous excitatory amino acid neurotransmitters, acting at AMPA receptors, tonically inhibit both TIDA and PHDA neurons, and thereby increase the secretion of prolactin and alpha-MSH in male and female rats.

5-Hydroxytryptamine2 receptor-mediated regulation of periventricular-hypophysial dopaminergic neuronal activity and the secretion of alpha-melanocyte-stimulating hormone.

The present study examined the effects of the 5-hydroxytryptaminergic (5HT)2/1c agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on periventricular-hypophysial dopaminergic (DA) neuronal activity and the secretion of alpha-melanocyte-stimulating hormone (alpha MSH). For comparison, the effects of DOI on tuberoinfundibular DA neuronal activity and the secretion of prolactin were also examined. Periventricular hypophysial and tuberoinfundibular DA neuronal activities were estimated by measuring the concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the terminal regions of these neurons; i.e., in the intermediate lobe of the pituitary and median eminence, respectively. Acute administration of DOI produced dose- and time-related decreases in intermediate lobe DOPAC concentrations and corresponding increases in plasma alpha MSH concentrations. Pretreatment of animals with either the 5HT2/1c antagonist ritanserin or the selective 5HT2 antagonist alpha-phenyl-1-(2-phenylethyl)-4-piperidine methanol (MDL-11,939) blocked the DOI-induced decrease in intermediate lobe DOPAC concentrations and increase in plasma alpha MSH concentrations. Acute administration of DOI produced dose- and time-related increases in plasma prolactin concentrations but did not alter DOPAC concentrations in the median eminence. Furthermore, the DOI-induced increase in plasma prolactin concentrations was blocked by ritanserin, but not MDL-11,939 pretreatment. Taken together, these data suggest that DOI inhibits periventricular hypophysial DA neuronal activity and increases the secretion of alpha MSH by activating 5HT2 receptors, whereas the DOI-induced prolactin secretion is independent of a decrease in tuberoinfundibular DA neuronal activity and is most likely mediated by 5HT2/1c receptor activation.

Denervation of the rat posterior pituitary gland: validation of a stereotaxic method.

A stereotaxic surgical method was developed for interrupting the nerve fibres running through the rat pituitary stalk to the posterior pituitary gland without obliterating the hypothalamo-pituitary portal circulation. The pituitary stalk was compressed by the blunt tip of an L-shaped rotating knife. Successful operations produced mild diabetes insipidus, disappearance of arginine vasopressin from the neural lobe, accumulation of arginine vasopressin and neurosecretory material in the pituitary stalk and no infarction in the anterior lobe of the pituitary gland. In female rats, the oestrous cycle was only temporarily disturbed. Plasma prolactin and corticosterone levels were high during the first 24 h after the stalk compression but returned to normal baseline levels from the second day after the operation. One week after the operation plasma adrenocorticotropin and prolactin levels were in the control range while plasma alpha-melanocyte-stimulating hormone was elevated. Denervation of the posterior pituitary gland may help in studying the neural control of intermediate lobe function and the role of the neural lobe in various endocrine conditions, and may serve as a model for lesions of the pituitary stalk and formation of ectopic neurohypophysis in the human.

Increased neuroendocrine reactivity and decreased brain mineralocorticoid receptor-binding capacity in aged dogs.

The effects of aging on the regulation of the hypothalamus-pituitary-adrenocortical (HPA) system of the dog were investigated. For this purpose, we compared 11 healthy dogs, 11-14 yr old, with 14 young mature dogs, 18-24 months of age. Significantly higher basal HPA activity in the old dogs was indicated by their higher resting plasma concentrations of ACTH, alpha MSH, and cortisol over a 6-week period and higher cortisol excretion in 24-h urine. After stress by immobilization as well as by light electric foot shocks and after i.v. administration of 1 microgram/kg CRH, the old dogs had higher peak levels of ACTH and cortisol, but not of alpha MSH. The areas under the curve, corrected for the basal levels, for ACTH and cortisol after these challenges were also greater in the old dogs. The half-times to reach a 50% increment and a 50% decrement in the time-concentration curves of ACTH and cortisol were similar in old and young dogs. There were no differences between the old and young dogs in their response to i.v. administration of 0.01 mg/kg dexamethasone. The clearance of [14C]cortisol from plasma, as calculated in a two-compartment model, was significantly reduced in aged dogs. In the old dogs, the stress- and CRH-induced cortisol peaks were relatively higher than those of ACTH, and their adrenals weighed significantly more, suggesting chronic hyperadrenocorticotropism. Aging had a markedly different effect on the two types of corticosteroid receptors in brain and pituitary. The binding capacity of type II or glucocorticoid receptors (GRs) in the old dogs was unchanged compared with that in the young dogs in all investigated brain structures except the anterior pituitary, in which the number of GRs was increased up to 170%. Type I or mineralocorticoid receptor (MR)-binding capacity was largely decreased in the brain of old dogs. The MR levels in old dogs, expressed as a percentage of the corresponding levels in young dogs, were 34% in the dorsal hippocampus, 58% in the ventral hippocampus, 37% in the septum, and 54% in the hypothalamus. In the anterior pituitary, MR capacity was unchanged. There was no difference between Kd values of MR and GR binding in young and old dogs. We conclude that these aged dogs had elevated basal HPA activity, characterized by increased levels of basal ACTH and cortisol in plasma and of urinary cortisol excretion and by hyperreactivity of ACTH and cortisol secretion in response to challenge by stress or CRH.(ABSTRACT TRUNCATED AT 400 WORDS)

Evidence that hypothalamic periventricular dopamine neurons innervate the intermediate lobe of the rat pituitary.

The purpose of the present study was to provide neurochemical and endocrinological evidence that dopamine (DA) neurons terminating in the intermediate lobe of the rat pituitary originate in the periventricular nucleus of the hypothalamus. One week following surgical separation of the periventricular nucleus from the mediobasal hypothalamus, DA and 3,4-dihydroxyphenyl-acetic acid (DOPAC) concentrations in the intermediate lobe were reduced by 50%, and this was accompanied by an increase in plasma alpha-melanocyte-stimulating hormone (alpha-MSH) concentrations. In contrast, this procedure had no effect on concentrations of prolactin in the plasma, or DA or DOPAC in the median eminence, the region of the mediobasal hypothalamus containing terminals of tuberoinfundibular DA neurons. Electrical stimulation of the periventricular nucleus increased the ratio of DOPAC/DA in the intermediate lobe and reduced the concentrations of alpha-MSH in the plasma, whereas in these same animals the DOPAC/DA ratio in the median eminence and concentrations of prolactin in the plasma were unaltered. These results indicate that approximately 50% of all the DA neurons terminating in the intermediate lobe of the rat pituitary originate in or project through the periventricular nucleus of the hypothalamus, and that these DA neurons regulate the secretion of alpha-MSH from intermediate lobe melanotrophs.

Effect of PUVA on plasma and skin immunoreactive alpha-melanocyte stimulating hormone concentrations.

Plasma alpha-melanocyte stimulating hormone (alpha-MSH) concentrations were measured in patients receiving PUVA therapy as treatment for mycosis fungoides, and PUVA or UVB as treatment for psoriasis. Skin immunoreactive alpha-MSH was also measured in those patients who received PUVA. The mean plasma and skin alpha-MSH concentrations after 2-3 weeks of PUVA were not significantly different from pre-treatment values and showed no relationship either to skin type or to the degree of tanning that occurred in response to PUVA. Plasma alpha-MSH concentrations were also unchanged after UVB. There was also no short term change in plasma alpha-MSH concentrations in patients after receiving their first treatment with PUVA. It would appear that circulating and skin alpha-MSH levels are unaffected by UV and show no causal relationship to PUVA induced pigmentation.