Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In rats of both sexes, mating stimulates neuronal activity in forebrain areas that are also activated by stress. Hypothalamic cells in the arcuate (ARC) and paraventricular (PVN) nuclei synthesize hormones or peptides whose levels are altered by adrenalectomy. In this experiment, we examined whether the mating-induced expression of c-FOS in the forebrain is altered by adrenalectomy (Adx) in female rats. Ovariectomized females were adrenalectomized (Adx) or sham-operated (Sham), hormone-primed and mated 2 weeks after surgery. They received 15 intromissions (15I), 5 intromissions (5I) or 15 mounts without intromission (MO) from a male or were taken directly from their home cage (HC). Two hours after mating, rats were perfused with paraformaldehyde and their brains were collected and stained immunocytochemically for FOS protein. FOS-immunoreactive (FOS-IR) cells in the posterodorsal medial amygdala (MePD), bed nucleus of stria terminalis (BNST), ventromedial hypothalamus (VMH), medial preoptic area (mPOA), ARC and PVN were counted bilaterally. In Sham animals, intromissions produced significant increases in FOS above HC levels. In Adx animals, mating increased FOS activity in all areas. However, responses to 5I and 15I differed between Sham and Adx groups. In all areas, Shams showed either the highest FOS response following 15I or levels which were equivalent after 5I and 15I. In Adx animals, the greatest number of FOS-positive cells occurred after 5I, with the 15I group showing significant suppression of FOS below 5I levels in the VMH, mPOA, ARC and PVN. These results demonstrate that the adrenal modulates FOS responses to mating in the female rat and suggest that adrenal secretory products normally may decrease sensitivity to low levels of mating stimulation. These effects may be due to increased corticotropin-releasing hormone (CRH) or beta-endorphin in the hypothalamus after adrenalectomy.
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PMID:c-FOS expression in the forebrain after mating in the female rat is altered by adrenalectomy. 1280 76

Housing rats in an enriched environment improves functional outcome after ischemic stroke, this may reflect neuronal plasticity in brain regions outside the lesion. Which components of the enriched environment that are of greatest importance for recovery after brain ischemia is uncertain. We have previously found that enriched environment and social interaction alone both improve functional recovery after focal cerebral ischemia, compared with isolated housing with voluntary wheel-running. In this study, the aim was to separate components of the enriched environment and investigate the effects on some potential mediators of improved functional recovery; such as the inducible transcription factors nerve growth factor-induced gene A (NGFI-A) and NGFI-B, and the glucocorticoid and serotonin systems. After permanent middle cerebral artery occlusion, rats were divided into four groups: individually housed with no equipment (deprived group), individually housed with free access to a running wheel (running group), housed together in a large cage with no equipment (social group) or in a large cage furnished with exchangeable bars, chains and other objects (enriched group). mRNA expression of inducible transcription factors, serotonin and glucocorticoid receptors was determined with in situ hybridisation 1 month after cerebral ischemia. Rats housed in enriched or social environments showed significantly higher mRNA expression of NGFI-A and NGFI-B in cortical regions outside the lesion and in the CA1 (cornu ammonis region of the hippocampus), compared with isolated rats with or without a running wheel. NGFI-A and NGFI-B mRNA expression in cortex and in CA1 was significantly correlated to functional outcome. 5-Hydroxytryptamine receptor 1A (5-HT(1A)) mRNA expression and binding, as well as 5-HT(2A) receptor mRNA expression were decreased in the hippocampus (CA4 region) of the running wheel rats. Mineralocorticoid receptor gene expression was increased in the dentate gyrus amongst wheel-running rats. No group differences were found in plasma corticosterone levels or mRNA levels of glucocorticoid receptor, corticotropin-releasing hormone, 5-HT(2C) or c-fos. In conclusion, we have found that social interaction is a major component of the enriched environment regarding the effects on NGFI-A and NGFI-B expression. These transcription factors may be important mediators of improved functional recovery after brain infarctions, induced by environmental enrichment.
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PMID:Effects of postischemic environment on transcription factor and serotonin receptor expression after permanent focal cortical ischemia in rats. 1280 85

It was reported that adrenocorticotropic hormone stimulates melanogenesis in cultured melanocytes. Stress (high population density and restraint stress) induced a significant increase in adrenocorticotropic hormone levels in plasma and skin compared to control. The serum obtained from HR-1 x HR/De F1 female mice subjected to stress showed significantly increased tyrosinase activity in human melanocytes compared to that from nonstressed mice. The increase in tyrosinase activity was inhibited in the presence of 10 nM corticostatin, an adrenocorticotropic hormone inhibitor. The aim of this study was to examine whether adrenocorticotropic hormone released into the circulation under stressful conditions is associated with the regulation of ultraviolet-induced pigmentation. Mice divided into three groups were housed for 22 d under the following conditions: five mice per cage (control); 10 mice per cage (high population density); restraint stress 4 h per d. The animals were exposed to ultraviolet-B irradiation (72 mJ per cm2, thrice per wk). After ultraviolet-B irradiation, delayed tanning was marked in stressed mice. The number of dihydroxyphenylalanine-positive melanocytes also significantly increased in stressed animals. Pretreatment with 100 microg of corticostatin inhibited the augmentation of the stress-induced pigmentary response and the increase in dihydroxyphenylalanine-positive melanocytes after ultraviolet irradiation. Adrenocorticotropic hormone released by stress may activate tyrosinase in melanocytes, resulting in the augmentation of ultraviolet-induced pigmentation. These results suggest that adrenocorticotropic hormone is at least partly responsible for the sensitivity of the pigmentary response after ultraviolet irradiation under stressful conditions.
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PMID:Stress augmented ultraviolet-irradiation-induced pigmentation. 1283 77

Antagonists of the corticotropin-releasing hormone receptor type 1 (CRH-R1) are regarded as promising tools for the treatment of stress-related psychiatric disorders. Owing to the intricate relationship between CRH and serotonin (5-HT), we studied the effects of chronic oral treatment of C57Bl6/N mice with the CRH-R1 antagonist NBI 30775 (formerly known as R121919) on hippocampal serotonergic neurotransmission during basal (on 15th day of treatment) and stress (forced swimming; on 16th day of treatment) conditions by in vivo microdialysis. Given the important role of CRH in the regulation of hypothalamic-pituitary-adrenocortical (HPA) axis activity and behavior, the effects of NBI 30775 on dialysate-free corticosterone levels, and on home cage and forced swimming-related behavior were also assessed. Chronic administration of NBI 30775 (18.4+/-0.9 mg/kg/day) did not result in alterations in food consumption and body weight. NBI 30775 caused complex changes in hippocampal serotonergic neurotransmission. Whereas no effects on the diurnal rhythms of 5-HT and its metabolite 5-hydroxyindoleacetic acid were found, the responses of the neurotransmitter and its metabolite to 10 min of forced swim stress were reduced and prolonged, respectively. NBI 30775 did not change free corticosterone levels over the diurnal rhythm. Moreover, NBI 30775-treated mice showed a similar forced swim stress-induced increase in corticosterone as observed in the control group. No effects of NBI 30775 on home cage, and swim stress-related active behaviors (climbing, swimming) and immobility were found. Thus, whereas chronic antagonism of CRH-R1 did not compromise HPA axis performance and behavior, distinct changes in serotonergic neurotransmission developed. Owing to the important role of 5-HT in the pathophysiology of mood and anxiety disorders, the latter observation may contribute to the therapeutical efficacy of CRH-R1 antagonists in these illnesses.
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PMID:Altered serotonergic neurotransmission but normal hypothalamic-pituitary-adrenocortical axis activity in mice chronically treated with the corticotropin-releasing hormone receptor type 1 antagonist NBI 30775. 1291 60

A brief exposure to social defeat in male Syrian hamsters (Mesocricetus auratus) leads to profound changes in the subsequent agonistic behavior exhibited by the defeated animals. Following defeat in the home cage of an aggressive conspecific, male hamsters will subsequently fail to defend their home territory even if the intruder is a smaller, nonaggressive male. This phenomenon has been called conditioned defeat. In Experiment 1, we examined the duration of conditioned defeat by repeatedly testing (every 3-5 days) defeated hamsters with a nonaggressive intruder. We found that conditioned defeat occurs in all defeated male hamsters and persists for a prolonged period of time (at least 33 days) in the majority of male hamsters tested despite the fact that these animals are never attacked by the nonaggressive intruders. In Experiment 2, we examined whether conditioned defeat could be induced in female Syrian hamsters. While conditioned defeat occurred in some females, they displayed only low levels of submissive/defensive behavior and, in contrast to males, the conditioned defeat response did not persist beyond the first test. These results suggest that in male hamsters conditioned defeat is a profound, persistent behavioral change characterized by a total absence of territorial aggression and by the frequent display of submissive and defensive behaviors. Conversely, social defeat in female hamsters does not appear to induce long-term behavioral changes. Finally, in Experiment 3, we determined that plasma adrenocorticotropin-like immunoreactivity increases in females following social defeat in a manner similar to that seen in males, suggesting that the disparate behavioral reactions of males and females are not due to sex differences in the release of, or response to, plasma adrenocorticotropin.
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PMID:Conditioned defeat in male and female Syrian hamsters. 1460 51

The role of vasopressin, cosecreted with corticotropin-releasing hormone (CRH), in stress is debated, because both normal as well as reduced adrenocorticotropin hormone (ACTH) rise to an acute challenge has been reported in Brattleboro rats genetically lacking vasopressin (di/di). Because di/di pups could be born either from di/+ (heterozygous) or from di/di mothers, and maternal influence is known to modify adult responsiveness, we investigated whether the influence of maternal genotype could explain the variability. Adult rats from mothers with different genotypes were stressed with 60 min restraint and trunk blood was collected for measuring hormone content by radioimmunoassay at the end of stress. All offspring of di/+ mothers had similar ACTH responses to restraint, while the di/di rats born to, and raised by di/di mothers showed reduced ACTH reactivity to restraint. The di/di rats showed elevated water turnover and required a daily cage cleaning every day, which meant frequent handling. To offset the role of handling, all rats had daily cage cleaning in the next series, but the results were the same as in the first series. To investigate whether lactation, the behaviour of the mother or some other factor during the pregnancy is responsible for the differences, pups from di/+ dams were raised by di/di foster mothers and vice versa. We found that the genotype of parental mother is more important than that of the foster mother. The corticosterone and prolactin elevation normally seen after acute stress was unchanged by family history, maternal or personal genotype. Furthermore, in studies with mutant animals, the rearing conditions should be controlled by the experimenter. In experiments with Brattleboro rats, the use of homozygous and heterozygous rats from the same litters of di/+ dams and di/di males is recommended. Our results suggest that vasopressin is not indispensable for ACTH release, and that the di/di genotype of the parental mother can decrease the stress reactivity of the di/di Brattleboro rats.
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PMID:Maternal genotype influences stress reactivity of vasopressin-deficient brattleboro rats. 1463 71

Structural and social aspects of an environmental system can influence the physiology and behavior of animals occupying that system. This study examined the physiological effects of environmental enrichment (EE) with Kong Toys and Nestlets on stress-responsive hormones of the hypothalamic-pituitary-adrenal (HPA) axis under basal and mild stress conditions in singly housed, jugular vein-cannulated, male and female rats. Animals of both sexes housed with EE had significantly lower baseline adrenocorticotropic hormone (ACTH) and corticosterone (CORT) concentrations compared to those housed without EE. ACTH responses to the mild stress of saline injection were significantly lower in female rats housed with EE. Interaction with the Kong Toys and Nestlets appears to have provided the rats with a diversion from monotonous cage life, resulting in lower HPA axis activity before and after mild stress. These results are important because low, stable baselines are essential for accurately discerning pharmacological and other influences on the HPA axis.
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PMID:Environmental enrichment lowers stress-responsive hormones in singly housed male and female rats. 1464 47

Behavioral, hormonal and neuronal responses to prolonged exposure to the volatile components of essential oil (EO) extracted from citrus lemon were investigated in male and female rats. Animals were exposed to the lemon essence for 2 weeks while in their cage. Anxiety was then determined with the elevated plus-maze apparatus while nociception was evaluated with a phasic thermal pain stimulus (plantar test) and with a chemical pain stimulus (formalin test). At the end of the experimental sessions, brain areas were dissected to measure beta-endorphin (beta-EP) concentrations in the hypothalamus and periaqueductal gray matter (PAG). Blood samples were collected to determine corticosterone plasma levels. In both sexes, prolonged EO exposure decreased the time spent in the open arms of the plus-maze apparatus. EO-exposed males and females showed higher thermal nociceptive thresholds than controls when tested with the plantar test apparatus. EO exposure induced female-specific decreases in formalin-induced pain behaviors during the formalin test. beta-EP concentrations in the hypothalamus and PAG were affected by EO. Corticosterone was lower in EO-exposed animals of both sexes than in their controls. These results suggest that long-term exposure to lemon EO can induce significant, at times sex-specific, changes in neuronal circuits involved in anxiety and pain.
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PMID:Effects of long-term exposure of lemon essential oil odor on behavioral, hormonal and neuronal parameters in male and female rats. 1497 56

The hormonal response to stress is enhanced by oestrogen but inhibited by androgens. To determine underlying changes in activity of neuropeptide neurones in the paraventricular nucleus of the hypothalamus (PVN), we examined the effect of oestrogen and androgen treatment on restraint-induced c-fos mRNA, corticotropin-releasing hormone (CRH) heteronuclear RNA, and arginine vasopressin hnRNA expression in the PVN. Male rats were gonadectomized and injected with oestradiol benzoate (EB) or dihydrotestosterone propionate (DHTP; s.c., daily for 4 days). Rats were stressed by restraint for 10 min or 30 min before killing. Other rats were stressed for 30 min and then returned to their home cage for 20 min before killing. Corticosterone and adrenocorticotropic hormone responses to restraint stress were significantly greater in EB-treated rats and lower in DHTP-treated rats at the 30-min timepoint compared to controls. c-fos mRNA increases following stress were augmented by EB but inhibited by DHTP. CRH hnRNA expression increased significantly in the PVN in response to restraint stress, and this increase was augmented by EB treatment, but decreased by DHTP treatment. Vasopressin hnRNA expression was also increased in response to stress, and this increase was attenuated by DHTP. These findings indicate that gonadal hormones influence the reactivity of the hypothalamic-pituitary adrenal axis to stress.
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PMID:Androgen inhibits, while oestrogen enhances, restraint-induced activation of neuropeptide neurones in the paraventricular nucleus of the hypothalamus. 1504 58

The brain corticotropin-releasing hormone (CRH) circuits are activated by stressful stimuli, contributing to behavioral and emotional responses. The present study assessed anxiety-like responses and in vivo neurochemical alterations at the central nucleus of the amygdala (CeA) evoked by exposure to an unfamiliar (anxiogenic) environment. Also, the impact of anxiolytic treatments and those that affect CRH were assessed in this paradigm. Novel environment (new cage) markedly suppressed ingestion of a palatable snack. This effect was dose-dependently antagonized by diazepam and was utilized as an index of anxiety in the rodent. Although exposure to a novel environment also stimulated the in vivo release of CRH and glutamate at the CeA, various CRH antagonists (e.g. alphah-CRH, Calpha-MeCRH, CP-154,526, antisauvagine-30, preproTRH178-199) did not attenuate the stressor-elicited behavioral suppression, although Calpha-MeCRH was found to attenuate the freezing response elicited by contextual stimuli that were associated with previously administered footshock. Moreover, central infusion of CRH failed to suppress snack consumption in the home cage. Although diazepam had potent anxiolytic effects in this paradigm, this treatment did not prevent the stressor-associated release of CRH and glutamate at the CeA. Thus, while neural circuits involving CRH and/or glutamatergic receptors at the CeA may be activated by an unfamiliar environment, the data challenge the view that activation of these receptors is necessary for the expression of anxiety-like behavioral responses. Rather than provoking anxiety, these systems might serve to draw attention to events or cues of biological significance, including those posing a threat to survival.
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PMID:Does amygdaloid corticotropin-releasing hormone (CRH) mediate anxiety-like behaviors? Dissociation of anxiogenic effects and CRH release. 1524 95


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