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

The present study investigated the consequences of prenatal exposure to the 5-hydroxytryptamine (serotonin; 5-HT) uptake inhibitor fluoxetine on central 5-HT2A/2C receptors and receptor-mediated function in male and female progeny. Pregnant rats were administered saline or fluoxetine (10 mg/kg s.c.) daily from gestational day 13 through 20. All litters were fostered to non-treated lactating dams. Fluoxetine did not alter weight gain during pregnancy but did significantly decrease progeny weight at birth (-8%) and at postnatal day (PD) 70 (-14%). Progeny were tested at PD28 (males and females) and PD70 (males) by measuring: 1) (+/-)-[125I]4-iodo,2,5-dimethoxyphenylisopropylamine ([125I]DOI)-labeled 5-HT2A/2C receptors; 2) [3H]paroxetine-labeled 5-HT uptake sites; and 3) the stimulation of adrenocorticotropin, corticosterone and renin after a single injection of the 5-HT2A/2C agonist DOI (2 mg/kg s.c.) to provide an index of 5-HT2A/2C receptor function. At PD28, neither 5-HT2A/2C receptor density nor 5-HT2A/2C receptor-mediated endocrine responses were altered by prenatal exposure to fluoxetine. In contrast, at PD70, the maximal density of hypothalamic 5-HT2A/2C receptors was reduced significantly (-35%) in male progeny of fluoxetine-treated dams. Consistent with the reduction of 5-HT2A/2C receptors, the adrenocorticotropin response to DOI was attenuated markedly and selectively (-58%; P < .05) in PD70 progeny following prenatal exposure to fluoxetine. Basal levels of all hormones measured were unaffected by prenatal fluoxetine. Likewise, fluoxetine did not alter the number of hypothalamic 5-HT uptake sites or the binding of [125I]DOI to cortical 5-HT2A/2C receptors.
 ...
PMID:Delayed decreases in brain 5-hydroxytryptamine2A/2C receptor density and function in male rat progeny following prenatal fluoxetine. 818 30

By means of in situ hybridization and immunocytochemical techniques it has been possible to follow the prenatal development of glucocorticoid receptor (GR) messenger RNA (mRNA) expression and GR immunoreactivity (IR) in the rat brain from embryonic day (E) 15 to 22. A 700-base-pair GR cDNA fragment was used for RNA probe generation. In the immunocytochemical analysis a mouse monoclonal antibody (IgG2a) against the rat liver GR was used in combination with the indirect fluorescence technique or the avidin-biotin immunoperoxidase method. At E15 till E22 a moderate to strong GR mRNA signal was observed within the neuro-epithelium from the medulla oblongata to the telencephalon. A moderate to strong labelling was also present within the paraventricular hypothalamic nucleus, the arcuate nucleus, the nucleus raphe magnus, the nucleus raphe obscurus and the locus coeruleus. In these areas a weak to moderate nuclear GR IR developed in nerve cells 1 or 2 days after the appearance of the GR mRNA signal. From E15 the adenohypophysis showed the strongest expression of GR mRNA. At E17 a strong GR IR was especially demonstrated in the nuclei of many pituitary cells, some exhibiting adrenocorticotropin IR. The results open up the possibility that there exist active GR in embryonic life capable of regulating proliferation events within the adenohypophysis and the neuro-epithelia of the brain. This embryonic GR may modulate the development of inter alia neuro-endocrine areas such as the paraventricular and arcuate nuclei and arousal-related areas such as the central 5-hydroxytryptamine and noradrenaline neuronal systems. Provided that this embryonic GR is capable of becoming activated by glucocorticoids in fetal life, it may mediate several neurochemical and behavioural impairments caused by prenatal stress.
 ...
PMID:Prenatal development of glucocorticoid receptor gene expression and immunoreactivity in the rat brain and pituitary gland: a combined in situ hybridization and immunocytochemical analysis. 823 69

The purpose of this study was to examine the effects of both acute and chronic administration of the peripheral sympatholytic antihypertensive agent losulazine on central dopaminergic, noradrenergic, and 5-hydroxytryptaminergic neurons in the rat. For comparison, the acute effects of reserpine were also examined. Acute systemic administration of losulazine produced marked dose- and time-dependent decreases in dopamine and norepinephrine concentrations in regions outside the blood-brain barrier (i.e., the median eminence, intermediate lobe, and neural lobe), that were accompanied by an increase in plasma concentrations of prolactin and alpha-melanocyte-stimulating hormone. By comparison, losulazine caused a relatively modest, transient depletion of dopamine and norepinephrine (but not 5-hydroxytryptamine) in regions of the brain protected by the blood-brain barrier (i.e., the striatum, nucleus accumbens, and dorsomedial nucleus of the hypothalamus). In contrast to losulazine, acute systemic administration of reserpine caused a prolonged depletion of dopamine, norepinephrine, and 5-hydroxytryptamine in all brain and pituitary regions examined. These results suggest that regional differences in the response of aminergic neurons to acute administration of losulazine and reserpine reflect differences in the ability of these drugs to penetrate the blood-brain barrier. Chronic systemic administration of losulazine produced a similar decrease in dopamine and norepinephrine in the median eminence, intermediate lobe, and neural lobe, suggesting that tolerance does not develop to the ability of losulazine to deplete catecholamines in these regions. Chronic losulazine administration also decreased dopamine concentrations in the striatum, and norepinephrine concentrations in the dorsomedial nucleus, suggesting that losulazine may have cumulative effects on central catecholamine neurons terminating in these brain regions.
 ...
PMID:Comparison of the effects of losulazine and reserpine on central aminergic neurons. 823 58

To determine whether cocaine-induced deficits in serotonergic function are long-lasting, the neuroendocrine responses to the serotonin (5-hydroxytryptamine, 5-HT) releaser, p-chloroamphetamine were evaluated 1-8 weeks subsequent to 7 days of cocaine exposure (15 mg/kg b.i.d.). In cocaine-pretreated rats, the p-chloroamphetamine-induced elevations of prolactin and renin secretion were significantly reduced for 8 and 4 weeks, respectively. In contrast, the p-chloroamphetamine-induced elevation of adrenocorticotropic hormone (ACTH) secretion was at control values 1 week after cocaine exposure. The data suggest that some cocaine-induced deficits in serotonergic function are long-lasting.
 ...
PMID:Repeated exposure to cocaine produces long-lasting deficits in the serotonergic stimulation of prolactin and renin, but not adrenocorticotropin secretion. 824 63

To understand some of the mechanisms underlying the neuroendocrine and neurochemical changes associated with aging, we administered the serotonin [5-hydroxytryptamine (5-HT)] releaser and reuptake inhibitor d-fenfluramine (d-FEN; 0.0, 0.2, or 0.6 mg/kg/day, p.o) for 30-38 days to young (4 months) and old (22 months) F344 male rats. Rats were stressed by placement into a novel open field (OF) for 20 min before sacrifice. Control animals were sacrificed immediately upon removal from their home cage (HC). Old rats exhibited less (p < 0.05) exploratory behavior than young rats, which was not altered by treatment with d-FEN. Old HC rats also had higher (p < 0.05) basal plasma levels of adrenocorticotropic hormone (ACTH) and prolactin (PRL) than young HC rats. Old OF rats showed higher (p < 0.05) levels of ACTH and corticosterone (CORT) than young OF animals. A stress-induced increase in PRL secretion was not observed in old rats. Subchronic low-dose d-FEN normalized the enhanced ACTH and CORT responses of old animals to novelty. In addition to these endocrine changes, stress-induced increases in medial frontal cortex (MFC) dopamine (DA) and norepinephrine (NE) turnover also were observed. The increase in NE turnover was greater (p < 0.01) in old than in young rats. d-FEN treatment blocked the stress-induced increase in MFC NE but not MFC DA turnover in both young and old rats. These data support a role for 5-HT and/or NE in some age-related neuroendocrine perturbations and suggest that increased 5-HT neurotransmission can normalize the hyperactivation of the hypothalamo-pituitary-adrenal axis of old male rats.
 ...
PMID:Neuroendocrine and neurochemical responses to novelty stress in young and old male F344 rats: effects of d-fenfluramine treatment. 825

Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). 839 20

The present study determined whether interleukin-2 (IL-2) and IL-2 receptors are present in the adult rat hypothalamus. In addition, we determined whether IL-2 is involved in the regulation of neurotransmitter release from hypothalamic slices. In the hypothalamus, the highest levels of endogenous IL-2 and IL-2 receptors were localized to the median eminence and arcuate nucleus. Application of exogenous IL-2 to hypothalamic slices produced significant decreases of potassium (25 mM)-evoked [3H]noradrenaline release (24%) without significantly affecting the evoked release of [14C]glutamate, [14C]5-hydroxytryptamine, [3H]dopamine or [3H] gamma-amino butyric acid. In addition, IL-2 increased the potassium-evoked release of methionine-enkephalin (by 78%) and beta-endorphin (by 38%) from hypothalamic slices without affecting the release of leucine-enkephalin. In contrast, the spontaneous release of neurotransmitters and neuropeptides was not affected by exogenous IL-2. Overall, the findings of this study suggest that hypothalamic IL-2 is an endogenous neurokine that may be of consequence to the regulation of hypothalamic function.
 ...
PMID:Interleukin-2 regulates monoamine and opioid peptide release from the hypothalamus. 847 53

The cellular nature of the giant eosinophilic cells of tuber and of the cells comprising subependymal giant cell astrocytoma (SEGA) in tuberous sclerosis (TS) remains unclear. To assess the characteristics of these lesions, 13 tubers and 6 SEGA were immunohistochemically studied with glial and neuron-associated antigens. In addition to conventional ultrastructure, 6 tubers and 8 SEGA were subjected to immunoelectron microscopic study for glial fibrillary acidic protein (GFAP) and somatostatin. Eosinophilic giant cells of tubers were positive for vimentin (100%), GFAP (77%) and S-100 protein (92%); such cells were also found to a various extent to be reactive for neuron-associated antigens, including neurofilament (NF) proteins (38%) or class III beta-tubulin (77%). SEGA also showed variable immunoreactivity for GFAP (50%) or for S-100 protein (100%); NF epitopes, class III beta-tubulin, and calbindin 28-kD were expressed in 2 (33%), 5 (83%) and 4 (67%) cases, respectively. Cytoplasmic staining for somatostatin (50%), met-enkephalin (50%), 5-hydroxytryptamine (33%), beta-endorphin (33%) and neuropeptide Y (17%) was noted in SEGA, but not in tubers. Ultrastructurally, the giant cells of tubers and the cells of SEGA contained numerous intermediate filaments, frequent lysosomes and occasional rectangular or rhomboid membrane-bound crystalloids exhibiting lamellar periodicity and structural transition to lysosomes. Some SEGA cells showed features suggestive of neuronal differentiation, including stacks of rough endoplasmic reticulum, occasional microtubules and a few dense-core granules. Furthermore, in one case of tuber, a process of a single large cell was seen to be engaged in synapse formation. Intermediate filaments within a few cells of both lesions were decorated by gold particle-labeled GFAP antiserum. Within the tumor cells of SEGA, irregular, non-membrane-bound, electron-lucent areas often contained somatostatin-immunoreactive particles, whereas the latter could not be detected in tuber. The present study provides further evidence of divergent glioneuronal differentiation, both in the giant cells of tubers and the cells of SEGA. The findings of similar cells at different sites, including the subependymal zone, white matter ("heterotopias"), and cortex indirectly supports the idea that these lesions of TS result from a migration abnormality.
 ...
PMID:Tuber and subependymal giant cell astrocytoma associated with tuberous sclerosis: an immunohistochemical, ultrastructural, and immunoelectron and microscopic study. 854 29

A cell line has been established from human placentae at the first trimester of normal pregnancy. The cell line was obtained by culture of purified cytotrophoblast cells in serum-free medium supplemented with epidermal growth factor, insulin, dexamethasone and 0.1% bovine serum albumin. The cells can be subcultured for >30 passages in one to three splits. All the cells were mononuclear epithelial-like cells positive to cytokeratin 18, gonadotrophin-releasing hormone (GnRH), neuropeptide Y, neurotensin, leucine-enkephalin, dopamine and 5-hydroxytryptamine immunocytochemical staining. The cells secreted GnRH, progesterone and oestradiol (in the presence of testosterone) but little human chorionic gonadotrophin and no beta-endorphin. The cell line showed human karyotypes and had a population doubling time of 48 h in serum-free medium. However, the cells would stop growing in the medium containing fetal bovine serum. A normal cytotrophoblast cell line established in serum-free medium will be particularly useful in the study of cytotrophoblast cell proliferation and differentiation.
 ...
PMID:Establishment and characterization of a cytotrophoblast cell line from normal placenta of human origin. 867 49

The effect of acupuncture at life-saving point on the central nervous depressive action of anesthetics was investigated in rabbits. Stimulation with electroacupuncture (EA) inserted in Jen-Chung point, which is located at the mid-point on the upper lip, decreased the sleeping time induced by pentobarbital or propofol. However, this action of acupuncture was not modified by naloxone at the doses sufficient to block opiate receptors. Plasma beta-endorphin detected by radioimmunoassay was also not markedly changed in rabbits which received similar electrostimulation. Moreover, pretreatment with para-chlorophenylalanine at a dose sufficient to deplete endogenous 5-hydroxytryptamine (5-HT) failed to influence the action of EA. Mediation of endogenous opioids and/or 5-HT in this action of EA was then ruled out. Prazosin reversed the sleeping time decreasing action of acupuncture in a dose-dependent manner. Also, the action of acupuncture was eliminated in rabbits which received intracerebroventricular injection of guanethidine at a dose which could block noradrenergic nerve terminals. It is suggested that stimulation of Jen-Chung point through EA can activate noradrenergic neurotransmission in the brain, which in turn reduces the central nervous depressive activity of anesthetics.
 ...
PMID:Decrease of anesthetics activity by electroacupuncture on Jen-Chung point in rabbits. 878 39


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>