Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the neonatal rat spinal cord slice preparation responses of the dorsal horn interneurons to iontophoretic or bath application of methionine-enkephalin (ME), substance P (SP) and somatostatin (SS) were qualitatively similar to those obtained in intact spinal cord. Thus, SP powerfully excited almost all neurons tested (15/16), while ME and SS depressed neuronal discharges in 13/14 and 4/6 units respectively. In some dorsal horn neurons the iontophoretic application of ME caused a marked depression of the SP-induced excitation. Angiotensin II (AgII) had no effect on dorsal horn units (n = 8). In the slices perfused with a Ca2+-free, Mg2+-high Krebs solution the extracellularly recorded effects of ME, SP and SS were not significantly modified, suggesting that the peptides were acting directly on postsynaptic sites. The results also indicate that the in vitro rat spinal cord slice preparation can be successfully utilized for further studies on the cellular mechanisms of actions of neuropeptides, particularly in relation to synaptic transmission processes in the dorsal horn.
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PMID:Neonatal rat spinal cord slice preparation: postsynaptic effects of neuropeptides on dorsal horn neurons. 616 14

The effects of a porcine gastric fundic mucosal extract (molecular weight less than 10 000) has been compared with the effects of eight candidate gastrointestinal peptides on glucose absorption from the jejunum in a rat model. Bolus injection of the extract produced immediate and marked depression of glucose absorption. None of the candidate peptides tested produced this response, although somatostatin and substance P depressed absorption as a late phenomenon after 30 minutes. We conclude that the effects of the fundic extract are not reproduced by any of these candidate peptides. This strengthens the evidence for a novel gastrointestinal peptide, resident in fundic mucosa, which affects absorption from upper small bowel.
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PMID:Effects of porcine gastric fundic factor, somatostatin, substance P, glucagon, neurotensin, bombesin, VIP, motilin, and pentagastrin on jejunal glucose absorption in the rat. 618 32

Motilin, a gastrointestinal peptide recently detected in the rat brain, was capable of stimulating growth hormone (GH) release from dispersed anterior pituitary cells in a dose-related fashion. In initial experiments, the minimum effective concentration was 10(-7) M and the effect was specific for just GH. Subsequent experiments demonstrated that concentrations of synthetic motilin as low as 10(-9) M could significantly stimulate GH release. Only large IV doses (100 micrograms) of motilin significantly elevated circulating GH levels in vivo. However, administration of antiserum to porcine motilin (100 microliters, IV) significantly depressed plasma GH levels, suggesting a physiologic role for median eminence and hypothalamic motilin in the control of GH secretion. Furthermore, infusion of motilin into the third ventricle of conscious rats resulted in a significant depression of GH levels, suggesting an ultrashort loop feedback action of motilin on the release of motilin itself or somatostatin. In light of motilin's only minor structural similarity to human pancreatic tumor GH-releasing factor (GRF) and the ability of passive immunoneutralization of motilin to lower GH, this 22-amino acid peptide must now be considered a physiologic GRF.
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PMID:Motilin: a novel growth hormone releasing agent. 642 71

Experiments were conducted to determine the influence of the pancreatic hormones insulin, glucagon, and somatostatin on reticuloendothelial system (RES) phagocytosis both in vivo and in the isolated perfused livers of rats. Chronic pancreatic hormonal treatment consisted of twice daily injections SC of NPH insulin with doses ranging from 0.75 U on day 1 to 9.0 U on day 13 and unchanged doses of glucagon (200 micrograms) and somatostatin (50 micrograms). Chronic treatment with insulin significantly depressed by 48% intravascular phagocytosis of colloidal carbon administered IV at a dose of 8 mg/100 g, while glucagon and somatostatin stimulated macrophage endocytic function by 32% and 26%, respectively, compared to the control value. Acute treatment with the three pancreatic hormones at 30 min prior to carbon administration similarly produced insulin depression as well as glucagon and somatostatin stimulation of RES phagocytosis. Addition of the three hormones at near physiologic concentrations (20 ng/ml for insulin, 10 ng/ml for glucagon, and 5 ng/ml for somatostatin) to the recirculating perfusate of isolated perfused rat livers simultaneous with 24 mg of colloidal carbon likewise resulted in phagocytic reduction after insulin and enhancement after glucagon and somatostatin. Experiments involving insulin in vitro with isolated perfused livers as well as glucose replacement therapy concomitant with insulin in vivo demonstrated that hypoglycemia is not necessary for phagocytic depression by insulin while severe hypoglycemia in the perfusion medium is sufficient to depress carbon uptake by isolated perfused livers independent of insulin. Both pancreatic hormones and the level of glycemia seem to be important in modulating hepatic reticuloendothelial system phagocytosis.
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PMID:Modulation of hepatic reticuloendothelial system phagocytosis by pancreatic hormones. 676 38

The serotoninergic neuronal systems of the brain stem are involved in several processes, like sleep, anxiety and depression. Because of this, these systems have received a great deal of attention during the last few years. As a result, the raphe nuclei have been shown to contain a variety of substances in addition to serotonin. For example they were shown to contain GABA, noradrenaline, enkephalin, somatostatin, substance P and cholecystokinin. Additionally, neuropeptide Y and tirotrophine releasing factor have been found to colocalize with serotonin in the dorsal raphe nuclei. All these results have expanded our knowledge on the raphe nuclei and suggest that many other substances, apart from serotonin, could be involved in the regulation of processes such as sleep, anxiety and depression. Further experiments are necessary to test if this hypothesis is correct.
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PMID:[New concepts relating to histochemistry of the serotonergic neural systems of the raphe nucleus]. 748 82

Growth hormone (GH) plasma concentrations reflect a balance between stimulation via GH-releasing hormone and inhibition by somatostatin. Cholinergic agonists enhance GH release by inhibiting somatostatin secretion and in health, stimulated GH release undergoes diurnal variation. We investigated the influence of cortisol on pyridostigmine-induced GH responses by testing six patients with DSM-III-R major depression at 09.00 and 14.00 h. There were no differences in GH responses to pyridostigmine between 09.00 and 14.00 h despite a preservation of the circadian variation of cortisol levels. If cortisol plays an important role in regulating cholinergic activity one would expect the diurnal variation of pyridostigmine-induced GH release to be preserved. As it is not, a reasonable assumption to make is that the muscarinic supersensitivity observed in depression may be independent of the prevailing steroid milieu.
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PMID:Loss of the diurnal variation of pyridostigmine-induced growth hormone responses in depression: the effect of cortisol. 767 52

A previous study demonstrated that administration of phenobarbitone to male AP Wistar rats for up to 7 days caused alterations in labelling indices (LIs) in several different tissues (including a reduction of the endocrine pancreas population LI) as determined by immunohistochemical visualisation of 5-bromo-2'-deoxyuridine (BrdU) incorporation into S-phase nuclei. The primary objective of this study was to determine whether treatment with phenorbarbitone influenced the replicative states of specific cohorts of the islet (of Langerhans) cell population or generated a uniform depression of LI. Quantitation of the LIs of individual islet cell cohorts was achieved by utilisation of a dual immunohistochemical staining method for BrdU and islet hormones (insulin, glucagon and somatostatin) using a sequential peroxidase anti-peroxidase (PAP)/alkaline phosphatase anti-alkaline phosphatase (APAAP) method employing diaminobenzidine and New Fuchsin chromogens, respectively. We observed reductions, increases and no change in LIs of insulin-, glucagon- and somatostatin-positive cells, respectively. We conclude that the decreased LI of the insulin-positive cohort was not countered entirely by the LI increase in the glucagon-positive cohort due to the larger size of the former. Furthermore, the effects of phenobarbitone treatment are not manifested generally in the islet cell population but in the insulin- and glucagon-positive cohorts only. The causation of these effects is unknown but is likely to be due to enhanced carbohydrate and hormone metabolism. We believe that the visualisation and quantitation of replicating cells in specific hormone-positive cohorts of the islet cell population provide opportunities for understanding the influence of xenobiotics and disease processes on pancreatic function.
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PMID:Assessment of the labelling index of cohorts of the pancreatic islet cell population in phenobarbitone-treated male rats using a double immunohistochemical technique for 5-bromo-2'-deoxyuridine and pancreatic hormones. 771 55

Aging is accompanied by important changes in the production and secretion of hormones. These partly arise from changes in the peripheral endocrine glands themselves but are also partly the consequence of changes in the neuro-endocrine regulating centers of the hormone secretion. Considering e.g. the male gonads, we know that the reduced androgen secretion (and the diminished spermatogenesis) along the ageing process is the consequence of changes in the testes, such as the reduced number of Leydig- and Sertoli-cells, as well as a reduced testicular blood-perfusion. But on the other hand, it should also be partly ascribed to functional changes of the hypothalamohypophysis. This appears from the lowered circadian rhythms of the testosterone levels, the lower plasma levels of free testosterone, although the secretion capacity of the Leydig-cells and the gonadotrophs is maintained. This points to a lower feed-back set-point of the gonadostat. Moreover the amplitude of the LH impulses and the lower opioid tonus are decreased in elderly men. In aged people, the secretion of the adrenal cortex is essentially characterized by an age-related drop of the androgen secretion (DHEAS) and a lower androgens-response to ACTH. This demonstrates changes in the adrenal gland itself. On the other hand, the secretion of cortisol and the production rates of this hormone remain rather stable, although the feedback centre is less sensitive in old lab-animals. This is suggested by a longer lasting and higher cortisol secretion after stress. According to Sapolsky, this is the consequence of a drop in the number of corticoid receptors in the hippocampus, following a loss of neurons, which would be the result of repeated stress. This progressive deterioration of the feed-back locus by the final hormone is also called: "neurohumoral hysteresis". Signs of its existence in aged people can only be found in pathological cases, such as depression or Alzheimer's disease. The secretion of growth hormone, and its plasma levels, as well as their response to "Growth hormone releasing hormone" (GHRH) is severely reduced in old people. This does not appear to be the consequence of the decreased number of somatotropic cells in aged people but seems to be caused by an increased somatostatin secretion by the hypothalamus. It means that this reduced growth hormone secretion has mainly a central origin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Neuroendocrinological aspects of aging]. 780 2

Patients with Alzheimer's disease (AD) and major depression have been shown to have overlapping clinical symptoms and biological markers, including decreased concentrations of cerebrospinal fluid (CSF) somatostatin-like immunoreactivity (SLI), which may be related to alterations in the hypothalamic-pituitary-adrenal axis activity. As in prior studies, we found that CSF SLI was significantly decreased in a group of AD patients (N = 49) and a group of elderly patients with major depression (N = 18), as compared with 13 age-matched controls (F[2, 77] = 12.9, p < .001). In the present study, CSF SLI and CSF corticotropin-releasing factor correlated significantly within the group of AD patients (r = 0.49, p < .0004) and almost attained significance in the depressed patients (r = 0.47, p < .07). CSF SLI correlated significantly with urinary free cortisol within each patient group (r = -0.51, p < .03). Clinical measures of dementia severity and depression did not consistently correlate with CSF SLI in either patient group.
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PMID:CSF somatostatin in Alzheimer's disease and major depression: relationship to hypothalamic-pituitary-adrenal axis and clinical measures. 790 67

Neuropeptides were examined in relation to suicidal behavior and its repetition in depression. There were no significant differences between depressed patients who had or had not attempted suicide for cerebrospinal fluid (CSF) concentrations of neuropeptide Y, somatostatin, diazepam-binding inhibitor, GABA, or corticotropin releasing hormone. A 5-year follow-up was carried out. There were no significant differences between depressed patients who did or did not reattempt suicide during the follow-up or who had never attempted for CSF concentrations of any of the neuropeptides measured. These negative results suggest that these neuropeptides are probably not major determinants of suicidal behavior or its repetition in depression.
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PMID:Neuropeptides in relation to suicidal behavior in depression. 790 97


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