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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Salt glands of ducks were induced to secrete sodium through the ingestion of salt water. In salt-adapted animals the administration of melanocyte-stimulating hormone (MSH) produced a rise in the sodium excreted by the salt gland, an effect which was not mimicked by adrenocorticotropin. Studies in vitro using incubations of gland slices and radioactive sodium ion showed that MSH increased sodium efflux, indicating that it acted directly upon the gland. We have previously observed that MSH has no effect on the pigmentary system of the duck. It is proposed that in the evolutionary process this hormone has acquired new target tissues in these birds.
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PMID:Alpha-melanocyte-stimulating hormone stimulates sodium excretion in the salt gland of the duck. 133 Aug 7

Pretest exposure to novelty or injections of beta-endorphin can enhance passive avoidance (PA) retention (e.g., Izquierdo & McGaugh, 1985). Enhanced retention may result from a "state-dependent" match between the CNS state during test and the novelty-induced beta-endorphin state that is obtained during training in a novel apparatus. Our Experiment 1 suggests that, unlike PA, Pavlovian fear conditioning in a conditioned lick suppression (CLS) paradigm may be beta-endorphin "state-independent." Rats were given one tone-shock pairing in a novel environment. Baseline lick rates and CLS tested 48 h later in a familiar environment were not affected by pretest exposure to novelty and/or injections of 3.33 mg/kg naloxone HCl. In Experiment 2, the same rats were PA trained/tested in a new apparatus. Saline or naloxone injections and various exposure (novel, familiar, none) conditions preceded (1h) the 24-h retention test. Pretest exposure to novelty reduced retention and naloxone eliminated that deficit. In Experiment 3, naive rats given pretest exposure to novelty also showed a PA retention deficit. The results of Experiments 2 and 3 may complement rather than contradict previous findings. Pretest induction of a beta-endorphin state by novelty may either enhance state-dependent retrieval of a "weak" memory trace or make a "strong/well consolidated" training memory more vulnerable to retroactive interference from "new learning" during the pretest exposure period.
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PMID:Naloxone eliminates passive avoidance retention deficits produced by pretest exposure to novelty in rats. 164 63

In the following studies, we investigated the effects of 24-h maternal deprivation on the infant's hypothalamic-pituitary-adrenal system. Experiment 1 examined the effect of deprivation on the infant's corticosterone (CORT) response to adrenocorticotropin hormone (ACTH) injection. At all ages studied, deprivation resulted in a potentiation of the response. At some ages, deprived nontreated pups had higher CORT levels than nondeprived pups. Experiment 2 examined the ontogeny of the deprivation-induced stress response, and the capacity of the mother to inhibit it. From 8 days of age onwards, deprived animals showed a CORT response to saline injection that was either absent or far smaller in nondeprived pups. Saline-induced CORT secretion was diminished, or prevented, by returning the infant to its dam. Maternal reunion had no effect on ACTH-induced CORT elevations. Finally, Experiment 3 investigated the effects of deprivation over a more extended period of time. In maternally deprived pups, ACTH-induced CORT elevations persisted for at least 2 h following reunion, but by 6 h had returned to baseline. These data suggest that maternal factors are involved in the regulation of the responsiveness of the pup's hypothalamic-pituitary-adrenal system.
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PMID:Maternal regulation of the adrenocortical response in preweanling rats. 166 24

Three experiments were conducted to assess the retrieval effects of a single dose of beta-endorphin and of naloxone, and of the novelty-induced antinociception response in the developing rat. Wistar rats 30, 45, 60, and 90 days old from our breeding stock were used. Animals were trained and tested, with a 24-h interval between sessions, in a two-way active avoidance task (using 20 presentations of a 5-s, 1-kHz tone and a 0.4-mA footshock) or in a step-down inhibitory avoidance task (using a 60-Hz, 0.2-mA footshock). Saline (1.0 ml/kg), beta-endorphin (2.0 microgram/Kg), or naloxone (0.8 mg/kg), was administered ip immediately after training, and saline or beta-endorphin was administered 6 min before testing. The retrieval enhancing effects of post-training naloxone and pretest beta-endorphin, and the retrieval impairing effect of post-training beta-endorphin, were consistently observed only in 60- and 90-day-old rats, on both tasks. In a third experiment, another group of naive rats was placed for 2 min in a novel environment (the shuttlebox) and nociception was assessed by the tail-flick method. Novelty-induced antinociception was observed only for 60- and 90-day-old rats, and this response was cancelled by naloxone given 6 min before exposure to novelty. These results suggest that both the retrieval effects of naloxone and beta-endorphin, in the doses used, and the novelty-induced antinociception response, which are possibly dependent on the activity of hypothalamic beta-endorphin system, become established between 45 and 60 days postnatal in the rat.
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PMID:Retrieval effects of beta-endorphin and naloxone, and the novelty-induced antinociception in the developing rat. 205 93

In addition to its anorectic properties, dexfenfluramine may inhibit some manifestations of feeding-related reward. We attempted to verify this effect by measuring paw-lick latency on the hot plate test in rats conditioned to expect a palatable food. The involvement of variations in beta-endorphinergic, dopaminergic and serotonergic systems was assessed. Despite an inherent effect of increasing paw-lick latency, dexfenfluramine (1.5 mg/kg IP) partly reversed the expectancy-induced increase in this latency. Saline-treated "expectant" rats displayed elevated plasma beta-endorphin levels and reduced hypothalamic 5-HIAA/5-HT and DOPAC/DA ratios. Only the decrease in the DOPAC/DA ratio was reversed by dexfenfluramine, suggesting an involvement of the dopaminergic system in this dexfenfluramine-sensitive reward system.
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PMID:Reversal of a feeding-reward system by dexfenfluramine: neurochemical involvement. 208 21

The effects of salt loading and adrenalectomy on arginine vasopressin (AVP) mRNA levels in the paraventricular nucleus (PVN) and the supraoptic nucleus (SON) of the hypothalamus were studied by semiquantitative in situ hybridization histochemistry, using a synthetic oligonucleotide probe and a computer-assisted image analysis system. Salt loading (2% NaCl) for 7 days produced marked increases in AVP mRNA levels in the magnocellular neurons of the PVN, SON, and accessory nuclei. Adrenalectomy caused an increase in AVP mRNA expression in the magnocellular part of the PVN and the expansion of hybridization signals into its medial parvocellular region, where the cell bodies of corticotropin-releasing hormone (CRH) neurons are located. No apparent alteration of AVP mRNA levels was observed in the SON following adrenalectomy. These results indicate that hyperosmotic stimulation and the loss of circulating glucocorticoids had differential effects on AVP gene expression in the PVN and SON, and that the magnocellular PVN and SON neurons responded in different manners to the loss of feedback signals.
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PMID:Effects of hyperosmotic stimulation and adrenalectomy on vasopressin mRNA levels in the paraventricular and supraoptic nuclei of the hypothalamus: in situ hybridization histochemical analysis using a synthetic oligonucleotide probe. 226 Apr 95

The role of corticotropin-releasing factor (CRF) and opiocortin neuronal systems and a possible functional relationship between the two in the control of luteinizing hormone-releasing hormone (LH-RH) activity in the medial preoptic area (MPOA) for the regulation of lordosis behaviour were assessed in ovariectomised oestrogen-progesterone-treated female rats. Lordosis behaviour (assessed as the lordosis quotient) triggered by male mounting was significantly inhibited by either CRF or beta-endorphin infused into the MPOA in animals treated with normal doses of oestradiol benzoate (OEB) (5 micrograms) and progesterone (500 micrograms). Saline-treated animals exhibited high levels of lordosis. The inhibition of lordosis produced by either CRF or beta-endorphin could be reversed by LH-RH microinfusions into the MPOA. While naloxone pretreatment of the MPOA site prevented the inhibitory effects of beta-endorphin, neither the opiate antagonist nor anti-beta-endorphin-gamma-globulin (even in high concentrations) infused into the MPOA was effective in completely preventing the inhibition of lordosis produced by CRF. These findings suggest that the inhibition of LH-RH neuronal activity and lordosis behaviour by CRF may be due to a direct action and may not be the result of activation of beta-endorphin release. The possibility that the two peptidergic systems may act in a synergistic fashion is supported by the data showing that combined CRF-beta-endorphin treatment in the MPOA completely abolished lordosis. This is further supported by the finding that CRF totally abolished lordosis in animals pretreated with anti-corticotropin (ACTH-gamma-globulin although this result could suggest that CRF could preferentially stimulate the release of ACTH in the MPOA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of lordosis behaviour in the female rat by corticotropin-releasing factor, beta-endorphin/corticotropin and luteinizing hormone-releasing hormone neuronal systems in the medial preoptic area. 301 71

To investigate the chronic effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on aldosterone secretion, synthetic alpha-MSH (8 micrograms/day) was infused in Sprague-Dawley rats by miniosmotic pumps for 5 days. Saline was infused in equivalent volume for 5 days using the same type of pumps in the control group of rats. Aldosterone secretion from the capsular cells of the two groups was examined in the basal state and in response to various stimuli of aldosterone secretion. Aldosterone secretion in vitro from the alpha-MSH-treated rats was significantly impaired in response to all stimuli tested including cyclic AMP, suggesting an intracellular defect in aldosterone synthesis in that group. These results are similar to those observed after chronic adrenocorticotropin administration.
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PMID:Impaired aldosterone secretion from dispersed adrenal capsular cells of chronically alpha-MSH-treated rats. 303 59

The material presented here summarizes the bulk of the presently available immunologic data bearing upon the in vivo relationship between brown adipose tissue and the immune system. The experiments were carried out in rats adipectomized (by surgical excision of the interscapular brown adipose tissue at birth), thymectomized (by neonatal removal of the thymus), adipectomized and thymectomized, and corresponding sham-operated controls. The following immune phenomena were studied: antibody production to soluble and corpuscular antigens; Arthus and delayed hypersensitivity skin reactions to bovine serum albumin; rejection of allogeneic skin and thyroid grafts; lymph node enlargement in a host-versus-graft reaction; experimental allergic encephalomyelitis and thyroiditis; immune response in normal animals treated with extracts from brown adipose tissue; allergic encephalomyelitis in thymoadipectomized animals; plaque-forming cell response and hemagglutinating antibody titers in animals injected with met-enkephalin and leu-enkephalin; and survival rate of adipectomized mice inoculated with Sarcoma-I cells. The results indicated that the cell-mediated immune reactions were potentiated in adipectomized rats. Antibody production was not significantly changed by neonatal adipectomy. Adipectomized mice, inoculated with Sa-I tumor cells, survived longer than controls, thus indicating that adipectomy made possible the recognition of discrete histocompatible differences between Sa-I cells and A/JAX mice. Adipectomy increased the ability of rats to develop autoimmune diseases. Saline extracts from brown adipose tissue of newborn rats suppressed hypersensitivity skin reactions in normal adult rats. Thymoadipectomized rats showed an almost normal ability to develop allergic encephalomyelitis, a finding that suggested that the potentiating influence of adipectomy on encephalomyelitis was neutralized by thymectomy. It appears that brown adipose tissue functions as a natural antagonist of the thymus. Enkephalins were found to be more effective immunosuppressors in adipectomized than in normal animals. The last finding establishes a functional link between brown adipose tissue and neuropeptides. It seems that the potentiation of immune response in adipectomized animals is effected by altered release of yet unidentified mediators and modulators. The evidence indicates that brown adipose tissue, in which neurohumoral activity occurs, may be an important component of an integrated immunoneuroendocrine system.
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PMID:Brown adipose tissue. Its in vivo immunology and involvement in neuroimmunomodulation. 330 Apr 71

Corticotropin-releasing factor (CRF) stimulates the synthesis and release of adrenocorticotropin in the anterior pituitary and may help maintain fluid and electrolyte balance. 'Salt-loaded' rats had an increase in CRF mRNA in hypothalamic magnocellular neurons of the paraventricular and supraoptic nuclei and a decrease in message in the parvocellular paraventricular neurons. After salt-loaded rats were adrenalectomized, CRF mRNA increased in the parvocellular cells. In contrast to salt loading, water deprivation lead to a decrease in CRF mRNA in magnocellular and parvocellular neurons. These results show that CRF synthesis within separate populations of hypothalamic neurons is regulated differently under various conditions.
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PMID:Corticotropin-releasing factor mRNA in the hypothalamus is affected differently by drinking saline and by dehydration. 349 Apr 4


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