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 sensitivity (contractile response) to serotonin (5-HT) of the isolated rat uterus was increased either during estrus or by administration of estradiol to ovariectomized rats. These increases in sensitivity to 5-HT were specific, because the sensitivities to acetylcholine and oxytocin were not influenced in either case. Pargyline (10(-5) M), an inhibitor of monoamine oxidase, did not affect the contractile responses to 5-HT, acetylcholine and oxytocin of uterus from ovariectomized rats. The monoamine oxidase activities in 100,000 X g precipitates and supernatants of homogenates for uteri from ovariectomized rats were either increased or unchanged by administration of estradiol. The contractile response to 5-HT of the uterus of untreated ovariectomized rats was not affected by chlorimipramine at 10(-6) M, a concentration that inhibits 5-HT uptake. Administration of estradiol increased significantly the number of [3H]spiroperidol binding sites (5-HT receptors) from 0.56 +/- 0.04 to 1.23 +/- 0.11 pmol/mg of protein, but did not change the apparent affinity of 5-HT receptors. Administration of estradiol did not change the dissociation constant or number of binding sites for [3H]quinuclidinyl benzilate (muscarinic acetylcholine receptors) significantly. These results indicate that the specific increase in sensitivity to 5-HT on administration of estradiol is due to change in the number of 5-HT receptors, but not to change in 5-HT uptake or in metabolic degradation of 5-HT.
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PMID:Mechanisms of specific change by estradiol in sensitivity of rat uterus to serotonin. 653 99

The effects of graded amounts of centrally injected [intracerebroventricular, i.c.v.] oxytocin [OXT] have been studied on the steady-state level and pargyline-induced accumulation of serotonin [5-HT] in the hypothalamus, mesencephalon and dorsal hippocampus of rats. OXT only weakly affected the steady-state level of 5-HT. The pargyline-induced accumulation, on the other hand, was inhibited by central OXT treatment. Whereas OXT inhibited 5-HT accumulation in a dose-dependent manner in the hypothalamus, only the lowest amount of OXT was effective in the mesencephalon and the dorsal hippocampus. The data raise the possibility that an altered 5-HT metabolism is likely to have functional significance in the endocrine and behavioral effects of OXT.
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PMID:The influence of oxytocin on the steady-state level and accumulation of serotonin in rat brain regions. 671 60

The effect of lysine-8-vasopressin (LVP) and oxytocin (OXT) has been studied on the steady-state level of serotonin (5-HT),dopamine(DA) and norepinephrine (NE) in various brain areas four hours after intraventricular microinjection of the neuropeptides. LVP (50 microU) diminished in content of 5-HT and NE in the mesencephalon, the content of 5-HT in the septum as well as the content of DA and NE in the dorsal hippocampus. OXT (500 microU), on the other hand, decreased the content of 5-HT, DA and Ne in the hypothalamus, as well as the content of DA in the mesencephalon. In contrast, the septal NW level was increased following OXT treatment. The data indicate that both LVP and OXT are capable of influencing the 5-HT and catecholamine levels as late as 4 h after their administration. Therefore, our findings support the previous notion that posterior pituitary neuropeptides affect behavioral processes via interacting with the cerebral monoaminergic neurotransmission.
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PMID:Intraventricular administration of vasopressin and oxytocin effects the steady-state levels of serotonin, dopamine and norepinephrine in rat brain. 697 62

The effects of stimulation of supraoptic nucleus (SON) on the changes of oxytocin (OT), arginine vasopressin (AVP), norepinephrine (NE) and serotonin (5-HT) in the perfusate of locus coeruleus (LC) and changes of pain threshild (PT) were studied by methods of microinjection, radioimmunoassay (RIA) and high pressure liquid chromatography (HPLC) technique. The results showed that the OT contents at 30, 60 and 90 min after stimulation, that of AVP at 30 min and 5-HT at 60 min were increased significantly, while the NE contents at 30 and 60 min were decreased markedly. Injection of V1 antagonist into LC did not affect the analgesic effect caused by administration of L-glutamic acid (L-Glu) into SON, which, however, could be partially inhibited by V2 antagonist or even reversed by OT antagonist. The above results suggested that the analgesic effect due to stimulation of SON is caused by increase of 5-HT and decreases of NE in the LC though the action of OT released by SON on OT and V2 receptor in LC.
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PMID:[Role of locus coeruleus in analgesia caused by stimulation of supraoptic nucleus]. 748 72

The viral transneuronal labeling method was used in combination with immunohistochemical procedures to identify CNS neuropeptide and monoamine neurons that innervate the sympathetic preganglionic neurons (SPNs) which project to the stellate ganglion--the principal source of the sympathetic supply to the heart. Transneuronal labeling was found at three CNS levels: spinal cord, brainstem, and hypothalamus. In the thoracic spinal cord, apart from the pseudorabies virus (PRV)-labeled stellate SPNs, PRV-labeled neurons were localized in laminae I/II, IV, V, VII, and X as well as in the lateral spinal nucleus and lateral funiculus. In the C1-C4 spinal segments, labeled neurons were found in the lateral funiculus as well as laminae V and VII of the spinal gray matter. PRV-labeled cells were identified in lamina V and the dorsolateral funiculus of the lumbar spinal cord. Three medullary areas were consistently labeled: rostral ventromedial medulla (RVMM), rostral ventrolateral medulla (RVLM), and caudal raphe nuclei. The greatest concentration of labeling was found in the RVMM. This projection arose from adrenergic, serotonergic (5-HT), thyrotropin releasing hormone (TRH), substance P, somatostatin, enkephalin, and vasoactive intestinal peptide (VIP) immunoreactive neurons. The RVLM projection originated mainly from C1 adrenergic neurons, some of which contained immunoreactive neuropeptide Y (NPY). C3 adrenergic-NPY neurons lying near the floor of the 4th ventricle were also labeled. Enkephalin-, somatostatin- and VIP-immunoreactive RVLM neurons also contributed to this projection. 5-HT neurons of the caudal raphe nuclei (raphe pallidus, raphe obscurus, and raphe magnus) were labeled; some of these contained substance P or TRH-immunoreactivity with an occasional neuron staining for all three putative neurotransmitters. In the pons, catecholamine neurons in the A5 cell group, subcoeruleus and Kolliker-Fuse nuclei were labeled. The midbrain contained relatively few infected cells, but some were present in the Edinger-Westphal and precommissural nuclei. Forebrain labeling was concentrated in the paraventricular hypothalamic nucleus (PVN) with lesser amounts in the lateral hypothalamic area (LHA) and the perifornical region. In the PVN, oxytocin-immunoreactive neurons accounted for the greatest chemically-defined projection while corticotrophin releasing factor (CRF), vasopressin-, and angiotensin II-immunoreactive neurons provided successively lesser inputs. In the LHA, angiotensin II-immunoreactive neurons were labeled. In summary, this study provides the first detailed map of the chemically-coded CNS neurons involved in the control of the cardiosympathetic outflow.
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PMID:Transneuronal labeling of CNS neuropeptide and monoamine neurons after pseudorabies virus injections into the stellate ganglion. 755 33

The present study aimed to check the hypothesis concerning the monoamine regulation of the differentiation of their target neurons during ontogenesis. For this aim, neuropeptide gene expression has been evaluated by in situ hybridization in targets for monoamines, differentiating peptidergic neurons, after monoamine depletion in rats during prenatal or early postnatal periods. In the first series of experiments, the vasopressin (VP) and oxytocin (OT) mRNA concentrations were measured in the supraoptic nucleus (SON) of rat fetuses at the 21st embryonic day (E21) following daily (E13-E20) treatment with the inhibitor of the catecholamine (CA) synthesis, alpha-methyl-m(p)-tyrosine. Similar study was performed with rats at the 11th postnatal day (P11) after daily (P2-P10) treatment with alpha-methyl-m-tyrosine and the neurotoxin, 6-hydroxydopamine. In the second series of experiments, the effect of serotonin (5-HT) depletion by the inhibitor of the 5-HT synthesis, p-chlorophenylalanine, on the vasoactive intestinal polypeptide (VIP) mRNA level in the suprachiasmatic nucleus (SCN) has been studied in fetuses and in neonates as described above. No changes were detected in the VP and OT mRNA concentration in the SON following CA depletion in fetuses, while similar treatment of neonates significantly increased both mRNA levels. On the contrary, the 5-HT depletion caused an increased VIP mRNA concentration in the SCN in fetuses but not in neonates. Thus, our data suggest a monoamine inhibitory influence on peptide gene expression in the differentiating target neurons during certain periods of ontogenesis.
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PMID:Monoamine influence on neuropeptide gene expression during ontogenesis. 772 32

Annetocin, an oxytocin-related peptide recently isolated from the lumbricid earthworm Eisenia foetida, and putative transmitter substances were examined for their effects on rhythmic, spontaneous contractions of isolated gut preparations of the earthworm. Significant, dose-dependent effects of the following substances were observed: acetylcholine (ACh), gamma-aminobutyric acid (GABA), and dopamine were excitatory, while serotonin (5-HT) and octopamine were inhibitory. Annetocin, oxytocin, and vasotocin stimulated spontaneous contraction of the earthworm gut, annetocin being approximately 10-fold more potent than oxytocin or vasotocin. However, arginine-vasopressin (Arg-vasopressin), lysine-vasopressin (Lys-vasopressin), tocinoic acid (N-terminal hexapeptide fragment of oxytocin), and MSH release-inhibiting factor (MIF; C-terminal tripeptide fragment of oxytocin) did not show any effect on the earthworm gut motility. On the other hand, oxytocin, vasotocin, Arg-vasopressin, Lys-vasopressin, and tocinoic acid caused spontaneous contractions of isolated rat uterine preparations, where the potency was in this order, while annetocin and MIF exerted no oxytocic activity on the uterus. Dose-response relationship of the effects of annetocin and its related peptides on the annelid and mammalian systems shows that amino acid residue at the third position of these peptides is important for exertion of excitatory action on the smooth muscle systems. The results in the present study suggest that receptors for annetocin and for GABA on the earthworm gut, unlike those for ACh, desensitize during continuous exposure to these substances.
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PMID:Effects of annetocin, an oxytocin-related peptide isolated from the earthworm Eisenia foetida, and some putative neurotransmitters on gut motility of the earthworm. 779 Aug 42

The purpose of the present studies was to determine whether cells in the hypothalamic paraventricular (PVN) or supraoptic (SON) nuclei mediate the serotonergic stimulation of oxytocin secretion. The serotonergic stimulus consisted of injection of the 5-HT-releasing drug p-chloroamphetamine (8 mg/kg, IP). The validity of this approach was verified by comparing this drug with another 5-HT releaser, d-fenfluramine (5 mg/kg, IP). Both 5-HT releasers increased plasma oxytocin concentration. Furthermore, the 5-HT uptake blocker fluoxetine (10 mg/kg, IP) blocked the effects of both p-chloroamphetamine and d-fenfluramine on plasma oxytocin concentrations, suggesting that both 5-HT releasers must be taken up through the 5-HT transporter into 5-HT nerve terminals to increase oxytocin secretion. In the lesion experiments, cells in the hypothalamic PVN or SON were destroyed by injection of the cell-selective neurotoxin ibotenic acid. The PVN lesions reduced basal levels and inhibited the effect of p-chloroamphetamine (8 mg/kg, IP) on plasma oxytocin concentration. In contrast, SON lesions did not alter basal oxytocin levels and did not reduce the oxytocin response to p-chloroamphetamine, suggesting that the SON is not involved in the serotonergic stimulation of oxytocin secretion. Site specificity of the PVN lesions was confirmed when injections of ibotenic acid into the hypothalamic dorsomedial nucleus (DMN), immediately caudal to the PVN, potentiated the oxytocin response to p-chloroamphetamine, suggesting that the DMN exerts an inhibitory influence on the secretion of oxytocin. Taken together, the data suggest that the serotonergic stimulation of oxytocin secretion involves PVN, but not SON, oxytocin neurons.
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PMID:Hypothalamic paraventricular, but not supraoptic neurons, mediate the serotonergic stimulation of oxytocin secretion. 788 48

The present study had two objectives: (1) to provide information on neuroendocrine challenge tests that can lead to diagnostic tests in humans; and (2) to confirm our previous observation that chronic fluoxetine selectively inhibits serotonin (5-HT1A) receptor function. We determined the effect of chronic fluoxetine and desipramine (DMI) on the hormone response to ipsapirone, a 5-HT1A agonist and a potential anxiolytic drug. Ipsapirone increased oxytocin, adrenocorticotropic hormone (ACTH), corticosterone, and prolactin, but not renin or vasopressin concentrations in plasma. Chronic fluoxetine, but not DMI, significantly inhibited the effect of ipsapirone on plasma oxytocin, ACTH and corticosterone concentrations. Chronic fluoxetine also reduced the Bmax for 3H-8-hydroxy-2-(dipropylamino) tetralin (3H-8-OH-DPAT) labelled 5-HT1A receptors in the midbrain. Neither antidepressant altered the density or affinity of 5-HT uptake sites. In conclusion, the present results confirm our previous results using 8-OH-DPAT as a challenge, and suggest that chronic 5-HT uptake inhibition results in adaptive changes leading to decreased function of the 5-HT1A receptor system. Finally, because ipsapirone may be administered to humans, it might be usable to evaluate 5-HT1A receptor function in depressed patients.
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PMID:Attenuation of hormone responses to the 5-HT1A agonist ipsapirone by long-term treatment with fluoxetine, but not desipramine, in male rats. 799 56

1-(3-Chlorophenyl)piperazine (m-CPP) (0.1-4 mg/kg s.c.) and N-(3-trifluoromethylphenyl)-piperazine (TFMPP) (0.5-4 mg/kg s.c.), 5-HT1C receptor agonists, but not 8-hydroxy-dipropylamino-tetralin (8-OH-DPAT) (0.1 and 0.2 mg/kg s.c.), a 5-HT1A receptor agonist, induced penile erection and yawning with a U-inverted dose-response curve in male rats. The maximal effect was found with 0.5 mg/kg s.c. of m-CPP and with 1 mg/kg s.c. of TFMPP. The m-CPP (0.5 mg/kg s.c.) and TFMPP (1 mg/kg s.c.) responses were prevented by mianserin (0.2 mg/kg s.c.) and by ritanserin (1 mg/kg s.c.) given 15 min before m-CPP and TFMPP. In contrast, m-CPP- or TFMPP-induced penile erection and yawning were not antagonized by haloperidol (0.1 mg/kg s.c.) or by [d(CH2)5Tyr(Me)2,Orn8]vasotocin (5 micrograms i.c.v.). Apomorphine- and oxytocin-induced penile erection, but not yawning, was also antagonized by mianserin and less effectively by ritanserin. The results suggest that 5-HT1C receptor agonist-induced penile erection and yawning are not mediated by increased dopaminergic and/or oxytocinergic transmission, and raise the possibility that a neuronal dopamine-oxytocin-5-HT link is involved in the control of penile erection and not necessarily of yawning in male rats.
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PMID:Penile erection and yawning induced by 5-HT1C receptor agonists in male rats: relationship with dopaminergic and oxytocinergic transmission. 800 37


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