Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Frozen and paraffin sections of six species of trematodes: Schistosoma mansoni, S. mattheei, S. japonicum, Schistosomatium douthitti, Echinostoma paraensei and Fasciola hepatica have been incubated with antisera against leu-enkephalin, FMRF-amide, gastrin-17, luteinizing hormone releasing hormone, neurotensin, oxytocin, prolactin, substance P, thyroid stimulating hormone and cholecystokinin, using indirect immunofluorescence and biotin-avidin horseradish peroxidase detection systems. 2. Of the ten antisera tested, six (leu-enkephalin, FMRF-amide, gastrin-17, luteinizing hormone releasing hormone, substance P and cholecystokinin) showed significant immunoreactivity, primarily in the central and peripheral nervous system, and also perhaps in the osmoregulatory system of the three species of Schistosoma. 3. Immunopositive nerve fibers extended from ganglia to gut wall, uterus and vitelline follicles, and especially from subtegumental nerve plexi to sensory receptors on the surface or in dorsal nippled tubercles.
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PMID:Immunocytochemical localization of regulatory peptides in six species of trematode parasites. 290 70

Exogenous administration of cholecystokinin octapeptide (CCK) is known to decrease food intake and slow gastric emptying in humans and animals. Recent studies have shown that CCK stimulates neurohypophyseal secretion of oxytocin (OT) in rats and arginine vasopressin (AVP) in monkeys, and that gastric distention also stimulates OT release in rats. We therefore studied AVP and OT secretion in 14 normal subjects in response to meal-induced gastric distention and administration of CCK, both separately and in combination, to assess whether these stimuli similarly activated central neurohypophyseal pathways in humans. Neither plasma AVP nor OT concentrations increased after gastric distention produced by ingestion of a large meal. However, a dose-related increase in plasma AVP, but not OT levels, occurred after CCK administration, the threshold CCK dose being 0.05 micrograms/kg body weight. The AVP secretion in response to CCK administration was significantly correlated with subjective aversive symptoms quantified by use of a numeric scale (r = 0.61, P less than 0.001). In 12 of the 14 subjects plasma AVP levels increased in association with symptoms of epigastric pressure and discomfort before the onset of overt nausea or emesis. The combination of CCK and meal-induced gastric distention did not stimulate increases in plasma AVP levels in excess of those produced by CCK administration alone. The results demonstrate that AVP secretion resulting from emetic center activation often is a graded response that can begin in association with milder degrees of visceral discomfort before symptoms of overt nausea or emesis. In addition, the stimulation of AVP secretion by CCK administration, but not by meal-induced gastric distention in association with physiological satiety, suggests that some component of the anorectic effects of exogenous CCK in man likely results from activation of brainstem emetic centers.
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PMID:Neurohypophyseal secretion in response to cholecystokinin but not meal-induced gastric distention in humans. 292 13

Neuropeptides and biogenic amines known to be present in neurons or afferent terminals in the paraventricular nucleus (PVH), supraoptic nucleus (SON) and/or lateral hypothalamus (LH) were added to small areas of these structures obtained by micropuncture and cyclic adenosine monophosphate (cAMP) levels were measured. cAMP accumulation occurred in PVH, SON and LH in response to neuropeptides of the secretin family, such as vasoactive intestinal peptide (VIP) and in response to catecholamines. Bradykinin, alpha-melanocyte-stimulating (alpha-MSH), luteinizing hormone-releasing hormone (LH-RH), oxytocin and carbamylcholine stimulated cAMP accumulation selectively in one or two of the above structures. Glucagon, cholecystokinin (CCK), somatostatin (SRIF), corticotropin-releasing factor (CRF), thyrotropin-releasing hormone (TRH), adrenocorticotropin (ACTH), melanocyte-stimulating hormone (MSH), methionine enkephalin (Met-Enk), beta-endorphin, neurotensin, bombesin and angiotensin II did not effect cAMP levels while leucine enkephalin (Leu-Enk), arginine vasopressin and gamma-aminobutyric acid (GABA) elicited regionally selective decreases in basal levels of cAMP. When interactions between some of these compounds were measured, VIP and norepinephrine exerted a more than additive effect on cAMP elevation in the PVH, while the effect on cAMP of the SON and LH was additive.
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PMID:Interaction of neuropeptides and biogenic amines on cyclic adenosine monophosphate accumulation in hypothalamic nuclei. 300 57

Administration of lithium chloride and copper sulfate to adult monkeys caused marked elevations in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. Emesis was produced in five of the seven animals given these agents, in support of nausea as the main stimulus to AVP release. A similar pattern of AVP release without OT release was found after administration of cholecystokinin (CCK). Although most monkeys vomited in response to 10 micrograms/kg of CCK, a significant increase in plasma AVP levels also was produced with a dose of 1 microgram/kg, which did not produce emesis in any animal. These findings are in marked contrast with previous results in rats, which indicated that lithium chloride, copper sulfate, and CCK each stimulated OT rather than AVP release. Despite this interspecies difference, the significant neurohypophysial hormone secretion in response to both nausea-producing agents and CCK suggests that AVP secretion in monkeys, similar to OT secretion in rats, might reflect activation of central pathways mediating nausea and/or inhibition of food intake, even when overt illness is not produced.
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PMID:Vasopressin release in response to nausea-producing agents and cholecystokinin in monkeys. 303 8

Colocalization of thyrotropin-releasing hormone-like immunoreactivity with other neuroactive substances was examined immunohistochemically in colchicine-treated rat brains using double-staining or elution-restaining methods. Thyrotropin-releasing hormone-like immunoreactivity was shown to be located in the same neurons as: 1. enkephalin-, gamma-amino butyric acid- and tyrosine hydroxylase-, but not somatostatin-like immunoreactivity in the glomerular layer of the olfactory bulb 2. oxytocin- and cholecystokinin-, but not vasopressin-like immunoreactivity in the supraoptic nucleus 3. cholecystokinin-like immunoreactivity in posterior pituitary 4. enkephalin-like immunoreactivity in the perifornical area of the hypothalamus and 5. neuropeptide Y- and neurotensin-like immunoreactivity in the periaqueductal central grey. These findings provide further examples of coexistence of thyrotropin-releasing hormone with classical neurotransmitters and/or peptides in the rat central nervous system.
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PMID:Coexistence of TRH with other neuroactive substances in the rat central nervous system. 315 46

Systemic injection of the peptide hormone cholecystokinin (CCK) is known to inhibit food intake and gastric emptying, and to stimulate neurohypophyseal secretion of oxytocin (OT) in rats. Previous studies also have shown that surgical destruction of afferent fibers in the gastric vagus eliminates the inhibitory effects of CCK on food intake. The present experiments used capsaicin to destroy peripheral sensory fibers in rats, and confirmed the failure of CCK to inhibit food intake. Similarly, capsaicin pretreatment markedly attenuated the stimulatory effect of CCK on OT secretion and the inhibitory effect of CCK on gastric emptying in rats. These and other results suggest that in rats CCK acts on receptors located on afferent fibers in the gastric vagus and stimulates inhibition of gastric emptying predominantly via a vagovagal reflex arc through the brainstem.
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PMID:Capsaicin pretreatment attenuates multiple responses to cholecystokinin in rats. 319 2

Previous reports have demonstrated that systemic injection of cholecystokinin (CCK) in rats produces dose-related decreases in food intake, increases in neurohypophyseal secretion of oxytocin (OT), and decreases in gastric emptying. The present studies determined whether systemic injection of bombesin (BBS), another peptide that potently reduces food intake in rats, had similar effects on OT secretion and gastric emptying. Although BBS produces a dose-dependent inhibition of food intake, even very high doses did not significantly affect plasma OT levels and only slightly decreased rates of gastric emptying. Consequently, despite their similar inhibitory effects on food intake, BBS does not appear to activate the same network of central nervous system pathways as does CCK in rats. However, parallel studies in monkeys demonstrated that systemic injection of BBS was effective in stimulating neurohypophyseal secretion of vasopressin rather than OT, in a pattern both qualitatively and quantitatively analogous to the effects of CCK in this species. Together with previous findings that BBS more potently inhibits gastric emptying in primates than in rats, these results therefore also suggest the presence of significant species differences in the central mechanisms by which BBS acts to reduce food intake.
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PMID:Species-specific effects of bombesin on gastric emptying and neurohypophyseal secretion. 324 50

The effect of 15 defined neuropeptides on the mitogenic activation of lymphocytes from human thymus, guinea pig lymph nodes and rat spleen was investigated. Lymphocytes were incubated in the absence or presence of polyclonal T and B cell activators together with increasing doses of the neuropeptides, and harvested at 48 h of culture after pulse-labeling with 3H-thymidine to assess the DNA synthesis. A dose-related stimulatory effect on the spontaneous 3H-thymidine incorporation of human thymocytes was obtained with methionine-enkephalin (met-enk), motilin and neurotensin. Vasoactive intestinal polypeptide (VIP) and peptide HI (PHI) were inhibitory. A similar responsiveness was observed in cultures of phytohemagglutinin P (PHA)-activated human thymocytes. The low level of basal DNA synthesis of guinea pig lymph node cells was stimulated by VIP and inhibited by neuropeptide Y (NPY) and PHI. PHA-activated lymph node T lymphocytes were stimulated by neurotensin, bombesin and motilin, whereas NPY inhibited the thymidine uptake. The low rate of spontaneous DNA synthesis of rat spleen cells was increased in the presence of VIP. Met-enk stimulated both basal and dextran sulfate-activated splenic B cell proliferation, whereas PHI was inhibitory in both cases. The following peptides were found to be inactive in all the above assays: substance P, cholecystokinin-octapeptide, somatostatin, galanin, oxytocin, pentagastrin and gastrin-releasing peptide 1-27 and 14-27. Although the responses were generally of low magnitude and observed at high peptide concentrations, present study contributes to the understanding of possible mechanisms involved in interactions between the nervous and the immune system.
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PMID:Neuropeptide regulation of human thymocyte, guinea pig T lymphocyte and rat B lymphocyte mitogenesis. 349 94

Systemic administration of cholecystokinin octapeptide (CCK-8) prompts an abrupt increase in circulating levels of oxytocin (OXY) but not vasopressin (VP) in rats. The present study determined whether CCK-8 selectively stimulated OXY-secreting neurons in the hypothalamic supraoptic nucleus of pentobarbital-anesthetized male rats. Antidromically identified neurosecretory neurons were categorized into putative OXY- and VP-secreting cells on the basis of their firing patterns and response to peripheral baroreceptor activation. Of 36 OXY-secreting cells studied, 30 demonstrated a 50-200% increase in firing frequency within 2 min of administering CCK-8 by intravenous or intraperitoneal injection, whereas none of the eight VP-secreting neurons studied was activated. In related experiments, 4-10 ml of air were used to inflate an intragastric balloon in rats; 20 of 22 OXY-secreting neurons displayed an abrupt and readily reversible increase in firing frequency, whereas only 2 of 17 VP-secreting cells were activated. Gastric distension similarly elevated plasma OXY levels in unanesthetized rats with indwelling gastric cannulas. Together with previous findings that the effects of CCK-8 on OXY release were attenuated by gastric vagotomy, these observations clearly demonstrate the existence of a sensitive neural link between the stomach and the neurohypophysis in the rat.
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PMID:Cholecystokinin and gastric distension activate oxytocinergic cells in rat hypothalamus. 366 61

Oxytocin (OXY) and cholecystokinin (CCK) coexist in neurons of the supraoptic nucleus and the paraventricular nucleus of the hypothalamus of the rat (Cell Tissue Res., 221 (1981) 227-231). Behavioral analysis of one possible terminal field of the OXY-CCK coexistence, the caudal region of the mesencephalic ventral tegmentum, was undertaken to investigate the functional significance of this coexistence. Both OXY and CCK were found to induce grooming behaviors when microinjected into the ventral tegmental area (VTA) of awake rats. Combinations of one low and one higher dose of OXY and CCK yielded grooming scores which were not significantly different from grooming scores induced by each peptide alone. In this case of putative coexistence of two peptides without a 'classical' neurotransmitter, each peptide appears to have a behavioral function, and the interaction between the two peptides may be competitive.
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PMID:Oxytocin and cholecystokinin induce grooming behavior in the ventral tegmentum of the rat. 369 Mar 7


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