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

This review summarizes the revolutionary impact of brain peptides on our understanding of the nervous system and then discusses the localization, distribution, synthesis, receptor sites, and possible function of 32 brain peptides. The peptides are discussed in three subgroups: I) the opioid peptides, which include beta-endorphin, the enkephalins, and dynorphin; II) the pituitary releasing hormones, most of which are wide-spread in the brain and include corticotropin-releasing hormone, luteinizing hormone-releasing hormone, somatostatin, and thyrotropin-releasing hormone; and III) a selection of 12 other peptides potentially important for neurological function, including vasopressin, oxytocin, substance P, cholecystokinin, bombesin, neurotensin, renin, angiotensin, vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and calcitonin. Within each individual peptide section, the possible physiological roles in anterior pituitary hormone release, blood-flow regulation, feeding behavior, temperature regulation, nociception, memory and learning, and movement are reviewed. Further, where noted, the peptide findings in Huntington's, Alzheimer's, Parkinson's and psychiatric diseases are emphasized.
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PMID:Neuropeptides. 187 Jul 24

We studied trophic effects of angiotensin II, vasopressin, cholecystokinin, and oxytocin on explanted ventral spinal cord cultures from 13- and 14-day-old rat embryos. There was a significant neurite promoting effect of the spinal cord cultures by using angiotensin II, vasopressin, and cholecystokinin. Cholecystokinin had the most potent effect at any concentrations. The minimum effective concentration was 10(-8) M in angiotensin II and vasopressin and 10(-12) M in cholecystokinin, respectively. The effect of angiotensin II and vasopressin was dependent on concentrations. However, the rate and grade of neurite appearance did not correlate with the concentrations of cholecystokinin. Oxytocin had no neurotrophic effect at any concentrations. Our results demonstrated that angiotensin II, vasopressin and cholecystokinin have neurotrophic effects on the ventral spinal cord in cultures, and may be candidates for therapeutic trials of amyotrophic lateral sclerosis.
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PMID:Trophic effect of angiotensin II, vasopressin and other peptides on the cultured ventral spinal cord of rat embryo. 188 May 32

Data are presented to show that vasoactive intestinal peptide (VIP) is synthesized and secreted by the hypothalamus and anterior pituitary and that it participates in the regulation of pituitary functions. Immunoreactive VIP in the hypothalamus and pituitary is increased following estrogen treatment and adrenalectomy and is reduced in hyperprolactinemic states. The level of VIP mRNA in the hypothalamus is increased during lactation and sexual maturation, while that in the anterior pituitary shows a sexual dimorphism and is increased with estrogen treatment and hypothyroidism. All these findings suggest a physiological regulation of hypothalamic and pituitary VIP gene expression in relation to its potential role as a neuroendocrine hormone. Furthermore, VIP stimulates prolactin (PRL) release at concentrations attainable in the hypophyseal-portal blood. Passive immunoneutralization studies with anti-VIP antisera suggest that endogenous VIP acts at multiple loci in the hypothalamic-pituitary axis to regulate PRL secretion, interacting possibly with other regulators of PRL secretion such as estrogen, serotonin, cholecystokinin, prostaglandins, galanin and oxytocin. Regarding other pituitary functions, although VIP has been shown to release growth hormone, ACTH, and vasopressin in vivo and in vitro, the physiological significance of these findings remains to be determined.
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PMID:Vasoactive intestinal peptide in the hypothalamus and pituitary. 190 91

Neurohypophysial secretion of vasopressin (AVP) and oxytocin (OT) was studied in rats maintained under hyposmolar conditions for 10-24 days. Graded intravenous infusions of hypertonic saline solutions had no consistent effect on plasma AVP and OT levels until plasma sodium concentration ([Na+]) exceeded 130 mM, after which levels of both hormones increased as an exponential function of plasma [Na+]. Detectable increases in plasma AVP and OT began at significantly lower plasma [Na+] in hyposmolar rats than in normosmolar control rats (10.8 mM lower for AVP and 18.4 mM lower for OT). AVP and OT secretion in hyposmolar rats was also markedly blunted in response to nonosmotic stimuli, including acute and chronic hypovolemia and systemic administration of cholecystokinin. Cessation of 1-desamino-8-D-arginine vasopressin-induced antidiuresis resulted in an appropriately rapid correction of plasma [Na+] to normal levels within 24 h. Consequently, although chronic hyposmolarity caused a moderate downward resetting of the osmotic thresholds for AVP and OT secretion, it did not cause sustained deficits in osmoregulation. These results suggest that osmoreceptor activity is regulated to maintain extracellular fluid and plasma osmolality within narrow absolute ranges rather than responding to relative changes in osmolality.
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PMID:Vasopressin and oxytocin secretion in chronically hyposmolar rats. 192 21

Hunger and satiety appear to reflect the postabsorptive and absorptive phases of caloric homeostasis, respectively. However, only some of the signals that inhibit food intake can be related to caloric homeostasis. For example, decreases in food intake also are observed after administration of nauseogenic chemical agents, treatment with cholecystokinin (CCK), or dehydration. In each case, inhibition of food intake is correlated with induced decreases in gastric motility and increases in secretion of pituitary oxytocin in rats; in primates, including humans, vasopressin but not oxytocin is secreted. In contrast, meal-induced satiety increases gastric contractions and has little or no effect on neurohypophyseal hormone secretion in rats or human subjects. Nauseogenic toxins, CCK, and dehydration stimulate very different subjective states from satiety: LiCl elicits abdominal cramps, nausea, and vomiting, as does exogenous CCK in high doses, whereas dehydration elicits thirst. Thus, inhibition of eating may not be associated with satiety or reflect changes in caloric flux; noncaloric controls of food intake exist and may be accompanied by distinctive increases in neurohypophyseal hormone secretion and loss of gastric function.
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PMID:Caloric and noncaloric controls of food intake. 195 22

Identification of specific cell types is fundamental to interpreting single cell recording studies. The hypothalamic supraoptic nucleus (SON) contains phasic (putative vasopressin) cells and a mixed population of continuously firing vasopressin and oxytocin cells. We injected cholecystokinin (CCK-8; i.v.), which is known to release oxytocin but not vasopressin, to see if such injections might differentiate oxytocin from vasopressin cells. Recordings made, using the ventral surgical approach to the SON in female rats under urethane anaesthesia (1.3 g/kg) from 49 non-phasic cells showed that CCK-8 (20 micrograms/kg) excited 41. Twenty of these 41 cells were tested for their response to i.v. injections of phenylephrine (10 micrograms), which interrupts the firing of putative vasopressin cells, and none were inhibited. Only one out of 8 cells recorded from suckled, lactating rats which showed a burst of spikes just before reflex milk-ejection was inhibited by phenylephrine. Injections of CCK-8 also excited 4 out of four such 'milk ejection' cells. Cells activated by CCK, cells unaffected by phenylephrine, cells activated just before reflex milk-ejection and cells which fire continuously appear to be a single population, thus continuous firing gives a good indication that an SON cell secretes oxytocin.
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PMID:Identification of oxytoxin cells in the rat supraoptic nucleus by their response to cholecystokinin injection. 202 16

In food-deprived male rats IP injection of cholecystokinin octapeptide (CCK-8, 5 micrograms), ingestion of food or ejaculation caused a comparable increase in plasma concentrations of CCK-8 and inhibited food intake. IV injection of 0.1 microgram CCK-8 interrupted ongoing feeding and greatly increased plasma CCK-8 levels. Osmotic minipumps delivering 0.5 micrograms CCK-8/h implanted IP reduced meal size and caused a modest increase in plasma CCK-8 levels. Injection of 5 micrograms CCK-8 IP produced an abrupt but transient increase in plasma CCK-8 concentrations whereas plasma concentrations of CCK-8 increased gradually with feeding. Injection of 5 micrograms CCK-8 IP, but not feeding, caused a marked increase in plasma oxytocin levels. The suppression of feeding, but not the increase in oxytocin, induced by IP CCK-8 was reversed by ICV injection of the CCK antagonist proglumide in a dose (100 micrograms) which failed to affect food intake if injected IP. Deprivation of food decreased and feeding increased the concentration of CCK-like immunoreactivity in the CSF. It is suggested that CCK-8 inhibits feeding in physiological doses by a specific mechanism in which peripheral as well as central neural CCK is involved.
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PMID:Relationship between the concentration of cholecystokinin-like immunoreactivity in plasma and food intake in male rats. 208 18

Pharmacological doses of insulin (3-25 U/kg sc) elicited feeding and increased gastric motility in rats. In contrast, the glucose analogue 2-deoxy-D-glucose (2-DG), given ip in doses known to increase food intake, had dose-dependent effects on gastric motility: 100 and 200 mg/kg 2-DG increased gastric motility, whereas 500 mg/kg 2-DG virtually eliminated gastric contractions. This latter result resembled the known effects on gastric motility of cholecystokinin (CCK) and LiCl. Moreover, like CCK and LiCl, 500 mg/kg 2-DG stimulated pituitary oxytocin (OT) secretion, and its effects on gastric motility and OT secretion were potentiated by pretreatment with the opioid antagonist naloxone. In contrast, OT secretion was not affected by insulin-induced hypoglycemia with or without naloxone pretreatment. These results suggest that there are two components to the effects of 2-DG on gastric motility: an insulin-like excitatory component and a CCK-LiCl-like inhibitory component. The latter inhibitory component may be mediated by the paraventricular nucleus of the hypothalamus, which has already been implicated in the inhibitory control of gastric motility.
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PMID:Effects of glucoprivation on gastric motility and pituitary oxytocin secretion in rats. 220 80

Plasma levels of cholecystokinin were increased in response to suckling in lactating rats. Efferent electrical stimulation of the vagal nerve increased the concentration of cholecystokinin in plasma. Abdominal vagotomy was found to block the suckling-induced release of cholecystokinin. Furthermore, lesions to the lateral midbrain, which disrupt the oxytocin-mediated milk-ejection reflex, were shown to inhibit the increase in plasma cholecystokinin. These results show that the suckling-induced release of cholecystokinin into plasma in lactating rats is dependent upon the vagal nerves and the central neural structures concerned with milk let-down.
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PMID:Suckling-induced release of cholecystokinin into plasma in the lactating rat: effects of abdominal vagotomy and lesions of central pathways concerned with milk ejection. 225 Jan 51

The [Ca2+]i of individual neurosecretory nerve terminals loaded with the fluorescent probe fura-2 was monitored during depolarizing stimuli and in the presence of substances known to induce or block neurohormone release. Induction of membrane depolarization with elevated [K+] or veratridine led to a rapid increase in [Ca2+]i that was sensitive to block by substances which block voltage-sensitive L-type Ca2+ channels such as the dihydropyridine nicardipine and by D-888. Relaxin, cholecystokinin and enkephalin which have been reported to regulate vasopressin and oxytocin secretion at the nerve endings were without effect on basal [Ca2+]i or K(+)-stimulated increases in [Ca2+]i.
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PMID:Effects of membrane depolarization on intracellular calcium in single nerve terminals. 228 8


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