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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intracellular recording techniques were used to study the effects of methionine enkephalin and dynorphin(1-13) on normal circular smooth muscle of human and baboon jejunum. Tetrodotoxin-sensitive inhibitory junction potentials had a mean (+/- SEM) amplitude of 21 +/- 3.3 mV in human jejunum and 24.1 +/- 1.3 mV in baboon jejunum. In both species, exogenously added methionine enkephalin and dynorphin (1-13) decreased inhibitory junction potentials amplitude in a dose-dependent manner with methionine enkephalin being more potent. Both opioid peptides acted on receptors located on axons of intrinsic inhibitory nerves. The effects of both methionine enkephalin and dynorphin(1-13) were blocked by ICI-174,864, a selective delta-receptor antagonist. The selective delta agonist, cyclic [D-penicillamine2, D-penicillamine5]enkephalin, and the selective mu agonist, Try-Pro-NMePhe-D-Pro-NH2, (each 10 mumol/L) decreased inhibitory junction potential amplitude by 79% +/- 6.9% and 61% +/- 4.8%, respectively. The selective kappa agonist, [trans-3,4-dichloro-N-methyl-N-(2-91-pyrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate, (10 mumol/L) had no effect. Although direct postsynaptic opioid receptor blockade of the inhibitory neurotransmitter on the smooth muscle cell has not been ruled out, the authors believe these data suggest that delta and mu receptors were present on inhibitory motor nerves innervating the circular muscle and that methionine enkephalin and dynorphin(1-13) decreased release of inhibitory neurotransmitter(s) by acting on delta receptors.
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PMID:Opioids inhibit neuromuscular transmission in circular muscle of human and baboon jejunum. 167 37

The relationship between wet-dog shaking (WDS) and afterdischarge (AD) elicited by dorsal hippocampal stimulation was investigated. The number of the WDS during a 150-s observation period was 9.6 +/- 2.0 (mean +/- SEM) and no WDS was seen during the non-seizure period. The effects of morphine and neuroleptics on WDS and AD were also investigated. Morphine significantly inhibited the number of WDS elicited by hippocampal stimulation. Naloxone significantly antagonized the inhibitory effect of morphine. Haloperidol and chlorpromazine significantly and dose-dependently inhibited the number of WDS at very small doses. The inhibitory effect of chlorpromazine on WDS was not antagonized by pretreatment with naloxone. The present results suggest that central dopaminergic mechanisms may be important in WDS elicited by hippocampal stimulation. The effect of morphine on WDS is probably mediated via an opioid receptor having a modulating effect on central dopaminergic mechanisms.
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PMID:Effects of morphine and neuroleptics on wet-dog shaking behavior elicited by hippocampal stimulation in rats. 286 Jun 86

The role of the opioid receptor-endogenous opioid peptide system in mediating analgesia induced by nitrous oxide has been a controversial subject. Most previous studies provided only indirect evidence either to support or refute the involvement of opioid receptors and/or endogenous opioid peptides. To provide more direct evidence, we measured concentrations of five naturally occurring endogenous opioid peptides in third ventricular cerebrospinal fluid from eight acclimated dogs with chronically implanted ventricular catheters. Paired samples of cerebrospinal fluid were obtained from each animal when breathing room air or 66-75 vol% nitrous oxide in oxygen through a face mask. Endogenous opioid peptides were physically separated using reversed phase high-performance liquid chromatography and quantified using radioimmunoassays. Nitrous oxide inhalation increased cerebrospinal fluid concentrations of met5-enkephalin from a control value of 0.30 +/- 0.07 (mean +/- SEM, n = 8) to 42.4 +/- 8.1 pmol/mL (P = 0.0006). Increases ranged from 28 to more than 400 times the control value. Met5-enkephalin-arg6-phe7 concentrations also increased from 14.5 +/- 2.5 to 57.6 +/- 17.8 pmol/mL (P = 0.018). No significant changes were noted in concentrations of dynorphin A, dynorphin B, or beta-endorphin. These results directly support the hypothesis that nitrous-oxide-induced analgesia involves the proenkephalin-derived family of endogenous opioid peptides.
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PMID:Nitrous oxide selectively releases Met5-enkephalin and Met5-enkephalin-Arg6-Phe7 into canine third ventricular cerebrospinal fluid. 789 15

The role of endogenous opioid mechanisms in the pituitary-adrenocortical response to acute stress was investigated in a longitudinal study in cyclic female pigs before and after exposure to chronic stress (long term tethered housing). Challenge of loose-housed pigs with acute nose-sling stress for 15 min induced an activation of the hypothalamic-pituitary-adrenocortical axis, evidenced by a transient increase in plasma ACTH (peak height above basal, 98 +/- 12 pg/ml; mean +/- SEM) and cortisol (54 +/- 3 ng/ml) concentrations. Pretreatment with the opioid receptor antagonist naloxone (0.5 mg/kg BW, iv bolus) increased the challenge-induced ACTH and cortisol responses to 244 +/- 36 pg/ml and 65 +/- 5 ng/ml, respectively. This indicates that during acute nose-sling stress, endogenous opioid systems are activated that inhibit the pituitary-adrenocortical response. After exposure of the pigs to chronic stress (10-11 weeks of tethered housing), the challenge-induced ACTH response was attenuated, whereas the cortisol response remained unchanged, suggesting an increased adrenocortical sensitivity to circulating ACTH. In addition, pretreatment with naloxone induced a greater increment in the ACTH and cortisol responses in tethered pigs than in loose-housed pigs. As no such changes were found in control animals housed loose during the entire experimental period, this indicates that the impact of opioid systems had increased due to chronic stress. The increased impact of opioid systems during chronic stress may prevent excessive hypothalamic-pituitary-adrenocortical responses to acute stressors and, thus, may be of adaptive value.
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PMID:Chronic stress increases the opioid-mediated inhibition of the pituitary-adrenocortical response to acute stress in pigs. 789 56

A reduction in endogenous opioid inhibition (disinhibition) of GnRH secretion is thought to be permissive for the preovulatory GnRH/LH surge. There are no published studies of the effects of highly specific opioid receptor agonists on the LH surge in any species, and the relative importance of the opioid receptor subtypes mu, delta and kappa in the mechanism of disinhibition is unknown. In sheep, attempts to block the LH surge with opiates have been largely unsuccessful, and there is little evidence for reduced opioid inhibition during the GnRH/LH surge. The opioid receptor subtypes regulating PRL secretion in sheep are also unknown. Conscious, ovariectomized ewes with permanent third ventricular cannulae were injected with estradiol benzoate (EB) 50 micrograms or oil im (t = 0 h). In this model, EB elicits a time-delayed surge in LH secretion after 13-18 h. Jugular venous blood was sampled at half hourly intervals between-2 and 0 h and 10 and 26 h. From 12-20 h, infusions were made into the third ventricle of either the highly specific mu-agonist DAGO (10, 20 or 40 nmol/h), the delta-agonist DPDPE (40 nmol/h), the kappa-agonist U50488 (40 nmol/h) or saline (vehicle). In oil-treated animals (n = 4-6), DAGO infusion at 20 and 40 nmol/h reduced plasma LH whereas DPDPE or U50488 had no effect. In EB-treated animals (n = 6), DAGO (40 nmol/h) delayed the LH surge (mean +/- SEM time to surge onset 21.4 +/- 0.3 h vs. 14.0 +/- 0.4 h in controls, P < 0.0001). DAGO at 10 nmol/h did not alter surge onset and at 20 nmol/h had variable effects. DPDPE or U50488 did not affect LH surge timing or amplitude. All doses of DAGO increased plasma PRL, whereas DPDPE and U50488 had no effect. We conclude that, in ovariectomized ewes, activation of opioid mu-receptors, but not delta- or kappa-receptors, inhibits GnRH secretion, can block the estrogen-induced GnRH/LH surge and increases PRL secretion. The results are consistent with the disinhibition hypothesis.
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PMID:Effects of central administration of highly selective opioid mu-, delta- and kappa-receptor agonists on plasma luteinizing hormone (LH), prolactin, and the estrogen-induced LH surge in ovariectomized ewes. 875 28

We have examined the effects of a range of opioid receptor subtype selective agonists on K+ evoked glutamate release from perfused rat cerebrocortical slices. Dual application (S1 and S2) of K+ (46 mM) evoked dual monophasic glutamate release profiles. When areas under the release curves were calculated an S2/S1 ratio for control slices of 1.07 +/- 0.08 (n = 75) was obtained, this was reduced by 80% with EGTA (0.1 mM) treatment confirming the presence of a Ca2+ regulated release process, Morphine produced a dose-dependent inhibition of the S2/S1 ratio. At 1 microM this amounted to 78 +/- 12% (mean +/- SEM; n = 6). (D-Ala2,MePhe4,gly(ol)5)enkephalin (DAMGO; 60 +/- 12%, n = 6 at 1 microM), and spiradoline (53 +/- 14% at 1 and 71 +/- 11% at 100 microM, both n = 6) also inhibited glutamate release in a cyprodime (10 microM) and norbinaltorphimine (10 microM) reversible manner. (D-Pen2.5) enkephalin (DPDPE; 1 microM) was ineffective. All agents tested did not affect basal glutamate release. Collectively these data implicate a role for mu and kappa opioids in the control of evoked glutamate release and their potential for neuroprotective therapy.
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PMID:mu- and kappa-opioids inhibit K+ evoked glutamate release from rat cerebrocortical slices. 894 32

Previous work has shown that small additions of a phosphate glass (CaO-P2O5) can significantly enhance the sinterability and strength of hydroxyapatite. However, there are no quantitative phase analyses available for these materials which would provide indicators of biocompatibility and resorbability. Similarly, there is little information available about the mechanical properties, especially with high glass additions. In this study, the effects of sintering hydroxyapatite with phosphate glass additions of 2.5, 5, 10, 25, and 50 wt.% are quantified. Each composition was sintered over a range of temperatures, and quantitative phase analysis was carried out using XRD. In addition, the microstructures were studied using RLOM and SEM, and mechanical properties (Vickers hardness, KIC, and MOR) measured. These results may be used to indicate which compositions and processing conditions may provide materials suitable for use in hard tissue replacement. Composites containing up to 10 wt.% glass additions formed dense HA/TCP composite materials possessing flexural strength and fracture toughness values up to 200% those of pure HA. The HA/TCP ratio was strongly dependent on the percentage glass addition. Higher glass additions resulted in composites containing beta-TCP together with large amounts of alpha- or beta-calcium pyrophosphate, and having similar mechanical strengths to pure HA.
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PMID:A quantitative study of the sintering and mechanical properties of hydroxyapatite/phosphate glass composites. 985 84

Endogenous agonists acting at kappa-opioid receptors modulate the discharge activity of hypothalamic supraoptic nucleus vasopressin cells in vivo. Phasic activity in vasopressin cells is known to depend critically on intrinsic mechanisms involving post-spike depolarizing after-potentials and we hypothesized that inhibition of phasic bursting by an endogenous kappa-agonist may result from reducing the magnitude of depolarizing after-potentials. To investigate this possibility, intracellular sharp electrode recordings were obtained from supraoptic nucleus cells impaled in superfused explants of rat hypothalamus. Bath application of the selective kappa-agonist, U50,488H (0.1-1 microM), decreased the spontaneous firing rate of magnocellular neurosecretory cells (by 94. 0+/-4.5% at 1 microM, mean+/-SEM; P = 0.02, n = 4). U50,488H did not alter membrane potential (0.9+/-0.8 mV hyperpolarization at 1 microM, P = 0.17, n = 8) or input resistance (11.0+/-4.5% increase at 1 microM, P = 0.09, n = 5). U50,488H (0.1 and 1 microM, both n = 5) reduced depolarizing after-potential amplitude (by 29.9+/-9.3 and 78.0+/-10. 6%, respectively, P<0.001) in eight cells in which the baseline membrane potential was kept constant by dc-current injection and in which a depolarizing after-potential was evoked every 25-40 s by a brief (40-80 ms) train of 3-6 action potentials (the number of spikes in the trains was kept constant for each cell). Thus, kappa-opioid receptor activation reduces depolarizing after-potential amplitude in supraoptic nucleus cells and this may underlie the reduction in burst duration of vasopressin cells caused by an endogenous kappa-agonist in vivo.
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PMID:Kappa-opioid receptor activation inhibits post-spike depolarizing after-potentials in rat supraoptic nucleus neurones in vitro. 1052 Jan 32

Endomorphin (EM)-1 and EM-2 are opioid tetrapeptides, reported within the central nervous system, which have very high specificity and affinity for the mu-opioid receptor. We have used newly developed and well-characterised radioimmunoassays (RIAs) in combination with reversed-phase high-performance liquid chromatography (HPLC) to detect EM-1 and EM-2 immunoreactivity (ir) in rat immune tissues. Endomorphins were detectable in extracts of rat spleen (total EM-1-ir/spleen: 440+/-73 pg, mean+/-SEM, a=group of eight rats; EM-2-ir: 150+/-12 pg) and thymus (EM-1-ir: 152+/-18 pg, mean+/-SEM n=8; EM-2-ir: 156+/-28 pg). EM-2-ir was detectable in extracts of human spleen (338+/-196 pg/g tissue, n=3). Multiple peaks of EM-1-ir and EM-2-ir were observed in rat spleen and thymus extracts, and multiple peaks of EM-2-ir were observed in extracts of human spleen, following reversed-phase HPLC and RIAs. This is the first report of endomorphin immunoreactivity in tissues of the rat and human immune systems.
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PMID:Novel opioid peptides endomorphin-1 and endomorphin-2 are present in mammalian immune tissues. 1081 82

Langendorff rat hearts were used (i) to examine whether fentanyl reduces stunning, infarction or both, and (ii) to investigate if this protection is mediated by delta-opioid receptors and/or protein kinase C (PKC). In the stunning study, hearts were subjected to global ischaemia (20 min) and reperfusion. This did not produce infarction. Postischaemic mechanical function was measured in hearts treated with or without fentanyl (740 nM). Fentanyl did not affect postischaemic mechanical function. In the infarction study, the left anterior descending coronary artery was occluded for 35 min and infarct size was assessed by triphenyltetrazolium chloride staining. Hearts in the control group exhibited an infarct zone/area at risk (I/R) of 39 (SEM 5)%, whereas the I/R for the fentanyl group was 13 (2)%. When the hearts were treated with a delta-opioid receptor antagonist (naltrindole 1 nM) or a PKC inhibitor (chelerythrine 2 microM), the effect of fentanyl was abolished, with I/R of 37 (1) and 36 (2)% respectively. In our model, we conclude that fentanyl protects against infarction but not against stunning, and that the limitation of ischaemic injury is mediated by both delta-opioid receptors and PKC.
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PMID:Fentanyl reduces infarction but not stunning via delta-opioid receptors and protein kinase C in rats. 1084 38


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