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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the effects of adenosine on the stimulation of glucose oxidation and lipogenesis by oxytocin and insulin in rat epididymal adipocytes. The addition of adenosine deaminase (1 U/ml) to the assay medium reduced the maximal oxytocin response (glucose oxidation and lipogenesis) to between 25 and 50% of the maximum response in control cells. The maximal response to insulin was not appreciably affected under these conditions. The addition of adenosine (10 or 30 microM) increased the cell sensitivity to oxytocin by elevating the maximum rate of oxytocin-stimulated glucose metabolism. Adenosine also increased the cell sensitivity to insulin by decreasing its ED50. A change in ED50, however, was observed only when control or adenosine-treated cells were compared to adenosine deaminase-treated cells; but not when control and adenosine-treated cells were compared. On its own, adenosine also caused an appreciable increase in both glucose oxidation and lipogenesis (ED50 approximately equal to 3 microM adenosine). The difference in the effect of adenosine on oxytocin action, compared with the effect on insulin action, points to differences in the mechanisms by which insulin and oxytocin stimulate glucose metabolism in adipocytes.
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PMID:Adenosine modulation of fat cell responsiveness to insulin and oxytocin. 354 88

Adenosine 3':5' monophosphate3 (cAMP) and guanosine 3':5' monophosphate (cGMP) are known to participate in the regulation of proliferation and differentiation, the processes intimately associated with maturation of the neonate. We have therefore examined their content in the physiological nutrient of the mammalian neonate, the mother's milk. Widely fluctuating concentrations between 0.1 and 0.7, and between 0.01 and 0.15 nmol/ml, were found for cyclic AMP and cyclic GMP, respectively. Concentrations in human breast milk changed during the 5-to 15-min period of one nursing, during any 24-h period, and also during the total lactation period. Levels of cyclic GMP were generally less fluctuating and were lower during afternoon and evening; they were relatively high at the start of lactation and levelled off during the postpartum period. The ratio of the two cyclic nucleotides also fluctuated widely and was significantly different from the ratio determined on blood plasma collected at the same time. Oxytocin injection had no effect on cyclic AMP content of rat milk. The stomach content of the nucleotide in rat pups remained high for at least 1 h after suckling indicating that cyclic nucleotides remain available for intestinal absorption; whether they have any physiological function in the neonate will have to emerge from further studies.
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PMID:Cyclic nucleotides in breast milk. 625 24

1. The effects of adenosine on synaptic transmission in magnocellular neurosecretory cells were investigated using whole-cell patch-clamp recordings in acute rat hypothalamic slices that included the supraoptic nucleus. 2. Adenosine reversibly reduced the amplitude of evoked inhibitory (IPSCs) and excitatory (EPSCs) postsynaptic currents in a dose-dependent manner (IC50 approximately 10 microM for both types of current). 3. Depression of IPSCs and EPSCs by adenosine was reversed by the application of the A1 adenosine receptor antagonist 8-cyclopentyl-1, 3-dimethylxanthine (CPT; 10 microM). 4. When pairs of stimuli were given at short intervals, adenosine inhibitory action was always less effective on the second of the two responses than on the first, resulting in an increased paired-pulse facilitation and suggesting a presynaptic site of action. This observation was confirmed by analysis of spontaneous miniature synaptic currents whose frequency, but not amplitude or kinetics, was reversibly reduced by 100 microM adenosine. 5. CPT had no effect on synaptic responses evoked at a low frequency of stimulation (0.05-0.5 Hz), indicating the absence of tonic activation of A1 receptors under these recording conditions. However, CPT inhibited a time-dependent depression of both IPSCs and EPSCs induced during a 1 Hz train of stimuli. 6. Taken together, these results suggest that adenosine can be released within the supraoptic nucleus at a concentration sufficient to inhibit the release of GABA and glutamate via the activation of presynaptic A1 receptors. By its inhibitory feedback action on the major afferent inputs to oxytocin and vasopressin neurones, adenosine could optimally adjust electrical and secretory activities of hypothalamic magnocellular neurones.
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PMID:Adenosine-induced presynaptic inhibition of IPSCs and EPSCs in rat hypothalamic supraoptic nucleus neurones. 1054 29

Effects of adenosine on voltage-gated Ca(2+) channel currents and on arginine vasopressin (AVP) and oxytocin (OT) release from isolated neurohypophysial (NH) terminals of the rat were investigated using perforated-patch clamp recordings and hormone-specific radioimmunoassays. Adenosine, but not adenosine 5'-triphosphate (ATP), dose-dependently and reversibly inhibited the transient component of the whole-terminal Ba(2+) currents, with an IC(50) of 0.875 microM. Adenosine strongly inhibited, in a dose-dependent manner (IC(50) = 2.67 microM), depolarization-triggered AVP and OT release from isolated NH terminals. Adenosine and the N-type Ca(2+) channel blocker omega-conotoxin GVIA, but not other Ca(2+) channel-type antagonists, inhibited the same transient component of the Ba(2+) current. Other components such as the L-, Q- and R-type channels, however, were insensitive to adenosine. Similarly, only adenosine and omega-conotoxin GVIA were able to inhibit the same component of AVP release. A(1) receptor agonists, but not other purinoceptor-type agonists, inhibited the same transient component of the Ba(2+) current as adenosine. Furthermore, the A(1) receptor antagonist 8-cyclopentyltheophylline (CPT), but not the A(2) receptor antagonist 3, 7-dimethyl-1-propargylxanthine (DMPGX), reversed inhibition of this current component by adenosine. The inhibition of AVP and OT release also appeared to be via the A(1) receptor, since it was reversed by CPT. We therefore conclude that adenosine, acting via A(1) receptors, specifically blocks the terminal N-type Ca(2+) channel thus leading to inhibition of the release of both AVP and OT.
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PMID:Adenosine inhibition via A(1) receptor of N-type Ca(2+) current and peptide release from isolated neurohypophysial terminals of the rat. 1198 69

Pituicyte stellation in vitro represents a useful model with which to study morphological changes that occur in vivo in these cells during times of high neurohypophysial hormone output. This model has helped us establish the hypothesis of a purinergic regulation of pituicyte morphological plasticity. We first show that ATP induces stellation in 37% of pituicytes, an effect that is secondary to the metabolism of ATP to adenosine. Adenosine-induced stellation of pituicytes appears to be mediated by A(1)-type receptors. The effect is independent of intracellular calcium and does not involve the mitogen-activated protein kinase pathway. The basal (nonstellate) state of pituicytes depends on tonic activation of a Rho GTPase because both C3 transferase (a Rho inhibitor) and Y-27632 (an inhibitor of p160Rho kinase) can induce stellation. Lysophosphatidic acid, a Rho activator, blocks the morphogenic effect of adenosine dose-dependently. Using a specific RhoA pull-down assay, we also show that downregulation of activated RhoA is the key event coupling A(1) receptor activation to pituicyte stellation, via F-actin depolymerization and microtubule reorganization. Finally, both vasopressin and oxytocin can prevent or reverse adenosine-induced stellation. The effects of vasopressin, and those of high concentrations of oxytocin, are mediated through V(1a) receptors. Placed within the context of the relevant literature, our data suggest the possibility of a purinergic regulation of pituicyte morphological plasticity and subsequent modulation of hormone release, with these hormones providing a negative feedback mechanism.
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PMID:RhoA inhibition is a key step in pituicyte stellation induced by A(1)-type adenosine receptor activation. 1200 47

Pituicytes have long been suspected to play a role in the regulation of neurohypophysial hormone output. This role has been mainly ascribed to morphological changes in these cells and subsequent modifications of their tight structural relationships with surrounding nerve terminals and capillaries. These entirely reversible changes are brought about by physiological states such as parturition, lactation, or dehydration, and it was inferred that they should facilitate neurohormone output, based on concerted analyses of in vitro, in situ, and ex vivo experiments. Pituicyte stellation, the in vitro counterpart of these morphological changes, can be induced by beta-adrenergic or A1-adenosine receptor activation, and appears to result from inhibition of the small GTPase RhoA. Actin depolymerization is the key event allowing stellation. Vasopressin and oxytocin reverse stellation and return pituicytes to their basal shape by activating Cdc42, another small GTPase that reorganizes the actin cytoskeleton in a cortical position. Adenosine and neurohormones also have opposite actions on the efflux of taurine, a local messenger that is released by pituicytes in hypotonic conditions and accordingly inhibits vasopressin output from axon terminals. As adenosine is likely generated from endogenous ATP co-released with neurohormones and broken down by local ectoATPases, these data suggest a subtle balance between a positive and a negative feedback on vasopressin output operated, respectively, by adenosine and vasopressin to maintain hydromineral homeostasis. A theoretical scenario is presented to account for the putative sequence of pituicyte-related events following disturbance of the hydromineral system.
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PMID:Pituicyte modulation of neurohormone output. 1880 8

Oxytocin is an important modulator of human affiliative behaviors, including social skills, human pair bonding, and friendship. CD38 will be discussed as an immune marker and then in more detail the mechanisms of CD38 on releasing brain oxytocin. Mention is made of the paralogue of oxytocin, vasopressin, that has often overlapping and complementary functions with oxytocin on social behavior. Curiously, vasopressin does not require CD38 to be released from the brain. This review discusses the social salience hypothesis of oxytocin action, a novel view of how this molecule influences much of human social behaviors often in contradictory ways. The oxytocinergic-vasopressinergic systems are crucial modulators of broad aspects of human personality. Of special interest are studies of these two hormones in trust related behavior observed using behavioral economic games. This review also covers the role of oxytocin in parenting and parental attachment. In conclusion, the effects of oxytocin on human behavior depend on the individual's social context and importantly as well, the individual's cultural milieu, viz. East and West. ACRONYMS: ACC = Anterior Cingulate ADP = Adenosine diphosphate AQ = Autism Quotient cADPR = Cyclic ADP-ribose CNS = Central nervous system DA = Dopamine eQTLC = Expression Quantitative Trait Loci LC-NE = Locus Coeruleus-Norepinephrine MRI = Magnetic Resonance Imaging OFC = Orbitofrontal cortices OXT = Oxytocin RAGE = Receptor for advanced glycation end-products SARM1 = Sterile Alpha and toll/interleukin-1 receptor motif-containing 1 TRPM2= Transient Receptor Potential Cation Channel Subfamily M Member 2 AVP = Vasopressin.
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PMID:A Novel Role of CD38 and Oxytocin as Tandem Molecular Moderators of Human Social Behavior. 3236 Apr 14