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)

The effect of oxytocin (OT) and cholecystokinin octapeptide (CCK-8) on EA analgesia was studied in rats. The increase of 20.8-39.8% and 9.0-45.0% in pain threshold was observed respectively when ICV of CCK-8 or naloxone was combined with EA, these increases were lower than that in saline-EA group significantly, while the simultaneous ICV of OT and CCK-8 or OT and naloxone in combination with EA produced the increase of 76.2-116.6% and 41.8-104.5% in pain threshold separately. These results showed that only a small part in the role of OT enhancing EA analgesia was blocked by CCK-8 and naloxone. The data suggest that the role of OT in EA was not entirely dependent upon the endogenous opiate peptides.
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PMID:[Effect of oxytocin and cholecystokinin octapeptide (CCK-8) on electroacupuncture (EA) analgesia]. 128 28

1. Cholecystokinin is co-localized within the oxytocin- and, to a lesser extent, vasopressin-synthesizing magnocellular neurones in the hypothalamic supraoptic and paraventricular nuclei. These nuclei are also prominent binding sites for cholecystokinin. In the present study we used intracellular current- and voltage-clamp recordings from fifty-seven supraoptic nucleus cells, maintained in superfused explants of rat hypothalamus, to assess their membrane responses to exogenous cholecystokinin and define the nature of their cholecystokinin receptors. 2. In a majority of the fifty-seven cells tested, bolus infusions into the superfusion media of cholecystokinin fragments (maximum concentrations estimated at 0.3-15 microM) were followed within 1-5 s by a transient and reversible membrane depolarization. Active peptides included sulphated cholecystokinin octapeptide (26-33) (28 of 33 cells responded), non-sulphated cholecystokinin octapeptide (26-33) (21 of 25 cells responded), cholecystokinin tetrapeptide (30-33) (20 of 24 cells responded and caerulein (4 of 4 cells responded). None of five cells responded to cholecystokinin (26-28). Depolarizing responses to cholecystokinin analogues persisted in the presence of tetrodotoxin (0.2-0.4 microM), and in Ca(2+)-free solutions containing MnCl2 (2.5 mM). 3. Under voltage clamp, cholecystokinin fragments evoked an inward current accompanied by an increase in membrane conductance. The amplitude of the inward current varied linearly as a function of membrane voltage, with an extrapolated reversal potential of approximately -15 mV. Reversal potentials were not altered by chloride injection. These features suggest that cholecystokinin activates a non-selective cationic conductance. 4. Active cholecystokinin analogues were approximately equipotent in their depolarizing actions, a feature that supports the activation of cholecystokinin-B type receptors. Moreover bath application of 200 nM L-365,260, an antagonist with a high affinity for cholecystokinin-B receptors, reversibly attenuated the cholecystokinin-induced responses in four of six cells tested. 5. These observations indicate that cholecystokinin can directly influence the excitability of rat supraoptic nucleus neurones and provide evidence for an additional site where this peptide may act within the hypothalamo-neurohypophysial axis.
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PMID:Depolarizing action of cholecystokinin on rat supraoptic neurones in vitro. 130 81

A microperfusion system was developed to study detailed kinetics of adrenocorticotropic hormone (ACTH) secretion by dispersed rat anterior pituitary cells responding to various ACTH secretagogues. The system approaches hydrodynamics to square-wave stimuli and enables kinetic analysis of ACTH secretion with intervals as short as 5 sec. ACTH secretion initiated within 5 sec of exposure of the cells to corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT) or angiotensin II (A-II) and reached a maximum within 20-40 sec. CRF induced a plateau-shaped secretion of ACTH which remained constant as long as CRF was perifused. In contrast, the ACTH secretion responding to AVP, OT and A-II rose rapidly to a peak and fell to the baseline despite continued perifusion of these agents. There were two components of ACTH secretory response to AVP and OT. AVP had synergistic effect with CRF only if it was perifused simultaneously with CRF or immediately after CRF was stopped. The ACTH secretory response to A-II was greatly diminished when cells were exposed to AVP or OT before A-II perifusion. Prior exposure to A-II had no effect on the magnitude of the ACTH secretory response to either AVP or OT. Epinephrine, nor-epinephrine, gastrin-releasing peptide, atrial natriuretic factor and cholecystokinin stimulated no significant ACTH secretion in the microperfusion system, although some of them induced ACTH secretion by same cell preparation in static culture systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Physiological analyses of secretory kinetics of adrenocorticotropic hormone (ACTH) from anterior pituitary cells: development and application of a microperfusion system]. 131 80

The presence of 3 different neuropeptide mRNAs with a strict cell-specific expression in vivo was investigated in 13 tumor cell lines from neuroendocrine and in 23 tumor cell lines from non-neuroendocrine origin. Northern blots showed no expression of mRNA for vasopressin (VP) in the 36 tested cell lines. Very low oxytocin (OT) mRNA hybridization signals were detected in the rat pituitary tumor cell line GH4C2 and the rat pancreas tumor cell line RIN5. Both the rat pituitary tumor cell line AtT-20 and the human myeloid leukemia cell line K562, contained proopiomelanocortin (POMC) mRNA. The low incidence of VP, OT and POMC gene expression in the tested tumor cell lines was not influenced by treatments inducing differentiation. In contrast, the cholecystokinin (CCK) gene which is widely present in nervous and endocrine systems was abundantly expressed in the human primitive neuroepithelioma cell line SK-N-MC and its clonal derivative SK-N-MC-IX-C. The results indicate that the expression of neuropeptide genes is very rare in tumor cell lines. The lack of expression in undifferentiated cells agrees with the appearance of expression after day 13 of the embryogenesis when maturation of neurons begins.
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PMID:Survey of neuropeptide gene expression in tumor cell lines. 132 Aug 92

Systemic administration of cholecystokinin (CCK) or LiCl inhibits gastric motility and food intake in rats. Brain stem-projecting oxytocin (OT) neurons in the hypothalamic paraventricular nucleus (PVN) have been proposed to mediate the inhibitory effects of CCK and LiCl on gastric motility and food intake. In the present studies, we found that basal gastric motility was elevated in rats 12-20 h after knife-cut lesions of the PVN; however, this effect disappeared 3 days later. Furthermore, CCK and LiCl inhibited gastric motility at 12-20 h, 3 days, and 3 wk after PVN lesions, although their effects were blunted. Injection of the local anesthetic lidocaine into the PVN had effects similar to acute PVN lesions. In rats with PVN lesions, the inhibitory effects of CCK and LiCl on food intake were indistinguishable from those in sham-lesioned rats. We conclude that the PVN tonically inhibits gastric motility and that it participates in, but is not essential for, the inhibitory effects of CCK and LiCl on gastric motility and food intake in rats.
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PMID:Gastric motility and food intake in rats after lesions of hypothalamic paraventricular nucleus. 132 67

Previous experiments have shown that gastric motility is inhibited by microinjection of oxytocin (OT) into the dorsal motor nucleus of the vagus (DMN) in anesthetized rats, and that the inhibition of gastric motility after electrical stimulation of the hypothalamic paraventricular nucleus (PVN) is blocked by microinjection of an OT receptor antagonist directly into the DMN. As an extension of these observations, the present series of studies demonstrate that gastric motility in unanesthetized, freely moving rats was reduced both by intracerebroventricular (i.c.v.) administration of OT and by electrical stimulation of the PVN, and that both of these inhibitory effects were blocked by i.c.v. administration of an OT antagonist. Moreover, an OT antagonist administered i.c.v. alone caused an increase in baseline gastric motility. However, pretreatment with the same OT antagonist i.c.v. did not block the inhibitory effects of systemic LiCl or cholecystokinin on gastric motility in conscious rats. These results suggest that oxytocinergic neurons exert a tonic inhibitory effect on gastric motility in rats, but that the inhibitory effects of LiCl and cholecystokinin on gastric motility are not primarily mediated by parvocellular OT-containing neurons projecting from the PVN to the DMN.
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PMID:Gastric motility in conscious rats given oxytocin and an oxytocin antagonist centrally. 132 62

1. Magnocellular neurosecretory cells (MNCs) were isolated from the supraoptic nucleus of adult Long-Evans rats using an enzymatic procedure. Immunocytochemical staining with antibodies against vasopressin and oxytocin revealed that MNCs can be identified by size. The membrane properties of these cells were examined at 32-34 degrees C using intracellular recording methods. 2. Isolated MNCs displayed a mean (+/- S.E.M.; n = 109) resting membrane potential of -64.1 +/- 1.0 mV, an input resistance of 571 +/- 34 M omega, and a time constant of 8.7 +/- 0.4 ms. Measurements of specific resistivity and input capacitance revealed that the soma of these cells accounts for a mere 20% of their total somato-dendritic membrane in situ. 3. Voltage-current relations measured near -60 mV were linear negative to spike threshold. From more hyperpolarized membrane potentials, voltage responses to depolarizing current steps displayed transient outward rectification and delayed impulse discharge. 4. Action potentials (76.6 +/- 0.9 mV) triggered from an apparent threshold of -59.3 +/- 0.1 mV broadened progressively at the onset of spontaneous or current-evoked spike trains. Steady-state spike duration increased as a logarithmic function of firing frequency with a maximum near 25 Hz. These effects were abolished in Ca(2+)-free solutions. 5. In all cells, evoked spike trains were followed by a prolonged Ca(2+)-sensitive after-hyperpolarization. In contrast, only a small proportion (16%) of MNCs displayed spontaneous bursting activity or depolarizing after-potentials following brief current-evoked bursts. 6. Isolated MNCs responded to amino acids (glutamate and GABA) and to the neuropeptide cholecystokinin, indicating that receptors for these neurotransmitters are expressed postsynaptically by MNCs and are retained following dissociation. 7. Increasing the osmolality of the superfusing solution by 5-30 mosmol kg-1 caused a membrane depolarization associated with a decrease of input resistance and accelerated spontaneous spike discharge in each of thirty-six MNCs tested. Current-clamp analysis suggested that these responses resulted from the activation of a cationic conductance. Excitatory effects of hyperosmolality were not observed in non-magnocellular neurones (n = 6).
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PMID:Properties of supraoptic magnocellular neurones isolated from the adult rat. 136 42

1. The cardiac responses of isolated frog (Rana tigrina) atria to peptide hormones were studied. 2. Calcitonin gene-related peptide (CGRP), arginine vasotocin (AVT), bovine parathyroid hormone fragment (bPTH-(1-34)) and oxytocin (OXY) produced dose-related positive chronotropic and inotropic responses; atrial natriuretic peptide (ANP) was negative chronotropic and inotropic; cholecystokinin (CCK), vasoactive intestinal peptide (VIP) were without effects. 3. The dose-related responses under bPTH-(1-34) stimulation but not CGRP or AVT were attenuated in the presence of ANP (300 ng/ml, approximately 0.98 x 10(-7) M). As expected ANP decreased the basal AR and AT responses of the isolated atria and the inhibitory effects were dose-dependent. 4. As shown previously, propranolol blocked the atrial tension stimulated by bPTH (1-34) but did not alter the cardiac responses to CGRP and AVT. 5. In the presence of beta-adrenergic blocker (propranolol 10(-7) M) or ANP (10(-7) M), the AR and AT changes under ISO stimulation in the frog were also decreased. 6. These cardiac changes suggest the cardiac inhibitory effects of ANP are related to beta-adrenoceptor activity and ANP might be a beta antagonist.
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PMID:Cardiac activity of some peptide hormones in the frog, Rana tigrina. 136 98

Systemic administration of cholecystokinin (CCK) decreases gastric motility and stimulates pituitary secretion of oxytocin (OT). Although peripheral OT does not affect gastric function, increasing evidence suggests that central OT secretion acting within the dorsal vagal complex (DVC) can alter gastric motility. To evaluate whether systemically administered CCK is capable of activating oxytocinergic neurons projecting to the DVC, we utilized fluorogold retrograde labeling from the DVC in combination with c-fos and OT immunocytochemical staining to quantitatively analyze paraventricular nucleus (PVN) neurons of rats following injection of CCK at a dose known to cause maximal pituitary OT secretion (100 micrograms/kg i.p.). Our results showed that 2320 +/- 63 PVN neurons were retrogradely labeled from the DVC; 146 +/- 21 (6.3%) of these contained OT, and these cells were predominantly located in the medial parvocellular subdivision of the PVN. Of all retrogradely labeled cells, 671 +/- 112 (28.9%) expressed c-fos after CCK stimulation, and 68 +/- 14 of these (10.1%) contained OT. Approximately 50% of the OT-containing neurons retrogradely labeled from the DVC stained positively for c-fos. Many magnocellular OT neurons in the PVN that were not retrogradely labeled from the DVC also expressed c-fos after CCK stimulation. These results demonstrate that parvocellular OT neurons projecting to the DVC are co-activated along with magnocellular OT neurons projecting to the pituitary following administration of a large dose of CCK, and lend support to a possible functional role for OT as a central neurotransmitter that modulates vagal efferent traffic to the gastrointestinal tract.
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PMID:Cholecystokinin induces c-fos expression in hypothalamic oxytocinergic neurons projecting to the dorsal vagal complex. 137 8

The hypothalamo-neurohypophyseal tract is known to contain the classical neurohypophyseal hormones vasopressin and oxytocin. Additionally, dynorphin, methionine- and leucine-enkephalin, cholecystokinin (CCK), corticotropin-releasing factor (CRF), and galanin are co-stored with vasopressin and/or oxytocin. Recent immunohistochemical studies have revealed the existence of a low to moderate number of substance P-, vasoactive intestinal peptide (VIP)-, neuropeptide Y (NPY)- and somatostatin-immunoreactive nerve fibers within the rat neurohypophysis. VIP-, substance P- and NPY-immunoreactive fibers were distributed throughout the organ, whereas somatostatin-immunoreactive fibers were present in the proximal part of the organ. The positive nerve endings were either large in size resembling classical nerve terminals related to perivascular spaces, or smaller similar to peptidergic fibers as described in the CNS. These results indicate that these neuropeptides may be either co-stored with the classical neurohypophyseal hormones or contained in another system of afferents to the organ. The probably distinct functional roles of these neuropeptides in the physiology of the neurohypophysis are discussed.
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PMID:Non-vasopressinergic, non-oxytocinergic neuropeptides in the rat hypothalamo-neurohypophyseal tract: experimental immunohistochemical studies. 138 83


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