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1

Ruzicka, Bianca B., та Khem Jhamandas. "The K+-evoked release of [3H]acetylcholine from slices of rat globus pallidus: modulation by δ-opioid receptors". Canadian Journal of Physiology and Pharmacology 69, № 3 (1991): 414–18. http://dx.doi.org/10.1139/y91-063.

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Previous investigations have shown that the activation of δ-opioid receptors depresses the release of acetylcholine (ACh) in the rat caudate putamen. This finding raised the possibility that the release of ACh is similarly modulated in the globus pallidus, a region containing a distinct population of cholinergic neurons and enriched in enkephalinergic nerve terminals. In the present study the pallidal release of ACh was characterized and the effects of δ-opioid receptor activation on this release were examined. The results show that this release is stimulated by high K+ in a concentration- and
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2

Ruzicka, Bianca B., та Khem Jhamandas. "Depression of potassium-evoked striatal acetylcholine release by δ-receptor activation: inhibition by cholinoactive agents". Canadian Journal of Physiology and Pharmacology 66, № 12 (1988): 1487–92. http://dx.doi.org/10.1139/y88-243.

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To examine the role of δ-opioid receptors in the modulation of striatal acetylcholine (ACh) release, the action of D-Pen2,L-Pen5-enkephalin, a selective δ-opioid receptor agonist, was tested on [3H]ACh release from slices of the rat caudate–putamen. Slices, incubated with [3H]choline, were superfused with a physiological buffer and stimulated twice by exposure to a high potassium (K+) concentration. In the absence of a cholinesterase inhibitor, 1 μM D-Pen2,L-Pen5-enkephalin produced a 46 and 35% decrease in the release of [3H]ACh evoked by 15 and 25 mM K+, respectively. The depressant action o
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3

Lauro, Figueroa-Valverde, Rosas-Nexticapa Marcela, Mateu-Armand Virginia та ін. "Preparation of two Cyclobutadiene-steroid derivatives Theoretical Analysis of its Interaction with the μ, d, and k Opiod-receptors". Oriental Journal of Chemistry 34, № 6 (2018): 2689–702. http://dx.doi.org/10.13005/ojc/340601.

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The objective of this investigation was to develop two cyclobutadiene-steroid derivatives (compounds 6 or 7) to evaluate its theoretical interaction on µ, d, and k opioid-receptors. The synthesis of 6 or 7 was carried out using a series of reactions which involves. 1) addition/cyclization: 2) imination, 3) etherification and 4) oxy-functionalization. Chemical structure of all compounds was confirmed using elemental analysis and NMR spectra. In addition, a theoretical analysis on the interaction of compounds 6 or 7 with µ, d, and k opioid-receptors was evaluated using a docking model. The resul
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4

Manandhar, Preeti, Bridin Patricia Murnion, Natasha L. Grimsey, Mark Connor, and Marina Santiago. "Do gabapentin or pregabalin directly modulate the µ receptor?" PeerJ 9 (April 12, 2021): e11175. http://dx.doi.org/10.7717/peerj.11175.

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Background Pregabalin and gabapentin improve neuropathic pain symptoms but there are emerging concerns regarding their misuse. This is more pronounced among patients with substance use disorder, particularly involving opioids. Co-ingestion of gabapentinoids with opioids is increasingly identified in opioid related deaths, however, the molecular mechanism behind this is still unclear. We have sought to determine whether pregabalin or gabapentin directly modulates acute μ receptor signaling, or μ receptor activation by morphine. Methods The effects of pregabalin and gabapentin were assessed in H
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5

Madamba, Samuel G., Paul Schweitzer, and George Robert Siggins. "Dynorphin Selectively Augments the M-Current in Hippocampal CA1 Neurons by an Opiate Receptor Mechanism." Journal of Neurophysiology 82, no. 4 (1999): 1768–75. http://dx.doi.org/10.1152/jn.1999.82.4.1768.

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Most electrophysiological studies of opioids on hippocampal principal neurons have found indirect actions, usually through interneurons. However, our laboratory recently found reciprocal alteration of the voltage-dependent K+current, known as the M-current ( I M), by κ and δ opioid agonists in CA3 pyramidal neurons. Recent ultrastructural studies have revealed postsynaptic δ opiate receptors on dendrites and cell bodies of CA1 and CA3 hippocampal pyramidal neurons (HPNs). Reasoning that previous electrophysiological studies may have overlooked voltage-dependent postsynaptic effects of the opio
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6

Ji, J., W. Lin, A. Vrudhula, et al. "Molecular Interaction Between Butorphanol and K-opioid Receptor." Obstetric Anesthesia Digest 41, no. 1 (2021): 44. http://dx.doi.org/10.1097/01.aoa.0000732540.18281.53.

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7

Carpenter, Elisabeth, J. Paul Gent, and Chris Peers. "Opioid receptor independent inhibition of Ca2+ and K+ currents in NG108–15 cells by the K opioid receptor agonist U50488H." NeuroReport 7, no. 11 (1996): 1809–12. http://dx.doi.org/10.1097/00001756-199607290-00024.

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8

Huh, Joon, Garrett J. Gross, Hiroshi Nagase та Bruce T. Liang. "Protection of cardiac myocytes via δ1-opioid receptors, protein kinase C, and mitochondrial KATP channels". American Journal of Physiology-Heart and Circulatory Physiology 280, № 1 (2001): H377—H383. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h377.

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The objective of the present study was to investigate the role of δ1-opioid receptors in mediating cardioprotection in isolated chick cardiac myocytes and to investigate whether protein kinase C and mitochondrial ATP-sensitive K+(KATP) channels act downstream of the δ1-opioid receptor in mediating this beneficial effect. A 5-min preexposure to the selective δ1-opioid receptor agonist (−)-TAN-67 (1 μM) resulted in less myocyte injury during the subsequent prolonged ischemia compared with untreated myocytes. 7-Benzylidenenaltrexone, a selective δ1-opioid receptor antagonist, completely blocked t
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9

Nechaykina, Olga V., Denis S. Laptev, Sergei G. Petunov та Andrei S. Radilov. "The effect of β-endorphin on the functional parameters of the isolated heart and lymphatic vessels of the white rat". HERALD of North-Western State Medical University named after I.I. Mechnikov 11, № 2 (2019): 43–48. http://dx.doi.org/10.17816/mechnikov201911243-48.

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Objective. The work is devoted to the comparison of the mechanisms of β-endorphin action in isolated rat heart and lymphatic vessels.
 Materials and methods. The experiments were performed using the Langendorff System perfusion device (Panlab, Spain) and the multichannel wire myograph 620M (DMT). During the study, selective opioid receptor blockers, K + channel blockers were used.
 Conclusion. In the course of experimental studies it was found that the most likely target for β-endorphin in an isolated rat heart are δ-opioid receptors, in isolated lymphatic vessels of a rat - μ- and δ
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10

Finnegan, Thomas F., Shao-Rui Chen та Hui-Lin Pan. "μ Opioid Receptor Activation Inhibits GABAergic Inputs to Basolateral Amygdala Neurons Through Kv1.1/1.2 Channels". Journal of Neurophysiology 95, № 4 (2006): 2032–41. http://dx.doi.org/10.1152/jn.01004.2005.

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The basolateral amygdala (BLA) is the major amygdaloid nucleus distributed with μ opioid receptors. The afferent input from the BLA to the central nucleus of the amygdala (CeA) is considered important for opioid analgesia. However, little is known about the effect of μ opioids on synaptic transmission in the BLA. In this study, we examined the effect of μ opioid receptor stimulation on the inhibitory and excitatory synaptic inputs to CeA-projecting BLA neurons. BLA neurons were retrogradely labeled with a fluorescent tracer injected into the CeA of rats. Whole cell voltage-clamp recordings wer
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11

Heinricher, M. M., S. McGaraughty, and D. K. Grandy. "Circuitry Underlying AntiOpioid Actions of Orphanin FQ in the Rostral Ventromedial Medulla." Journal of Neurophysiology 78, no. 6 (1997): 3351–58. http://dx.doi.org/10.1152/jn.1997.78.6.3351.

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Heinricher, M. M., S. McGaraughty, and D. K. Grandy. Circuitry underlying antiopioid actions of orphanin FQ in the rostral ventromedial medulla. J. Neurophysiol. 78: 3351–3358, 1997. Several laboratories recently identified a 17 amino-acid peptide, termed “nociceptin” or “orphanin FQ (OFQ)”, as the endogenous ligand for the LC132 (or “opioid receptor-like1”) receptor. Taken together with the fact that the cellular effects of OFQ are to a large extent opioid-like, the close relationship between the LC132 receptor and known opioid receptors raised expectations that the behavioral effects of this
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12

Xiao, Guo-Sheng, Jing-Jun Zhou, Guan-Ying Wang, Chun-Mei Cao, Gui-Rong Li, and Tak-Ming Wong. "In Vitro Electrophysiologic Effects of Morphine in Rabbit Ventricular Myocytes." Anesthesiology 103, no. 2 (2005): 280–86. http://dx.doi.org/10.1097/00000542-200508000-00011.

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Background Morphine is widely used in patients undergoing surgical operations and is also reported to mediate cardioprotection of preconditioning. The current study determined effects of morphine at therapeutic to pharmacologic concentrations on cardiac action potential, L-type Ca2+ current (ICa.L), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1) in isolated rabbit ventricular myocytes. Methods Ventricular myocytes were enzymatically isolated from rabbit hearts. Action potential and membrane currents were recorded in current and voltage clamp modes. Results Morphine at
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13

Piros, Elemer T., Rew C. Charles, Lei Song, Chris J. Evans та Tim G. Hales. "Cloned δ-Opioid Receptors in GH3 Cells Inhibit Spontaneous Ca2+ Oscillations and Prolactin Release ThroughK IR Channel Activation". Journal of Neurophysiology 83, № 5 (2000): 2691–98. http://dx.doi.org/10.1152/jn.2000.83.5.2691.

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Opioid receptors can couple to K+ and Ca2+ channels, adenylyl cyclase, and phosphatidyl inositol turnover. Any of these actions may be important in the regulation of neurotransmitter and hormone release from excitable cells. GH3 cells exhibit spontaneous oscillations of intracellular Ca2+concentration ([Ca2+]i) and prolactin release. Activation of cloned δ-opioid receptors stably expressed in GH3 cells inhibits both spontaneous Ca2+signaling and basal prolactin release. The objective of this study was to examine a possible role for K+ channels in these processes using the patch-clamp technique
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14

Liu, Yuan‐Yuarn, Hung‐Tsung Hsiao, Jeffery C. ‐F Wang, Yen‐Chin Liu та Sheng‐Nan Wu. "Effectiveness of nalbuphine, a κ‐opioid receptor agonist and μ‐opioid receptor antagonist, in the inhibition of I Na , I K(M) , and I K(erg) unlinked to interaction with opioid receptors". Drug Development Research 80, № 6 (2019): 846–56. http://dx.doi.org/10.1002/ddr.21568.

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15

Piras, Sandra, Gabriele Murineddu, Giovanni Loriga та ін. "Biological Effects on μ-Receptors Affinity and Selectivity of Arylpropenyl Chain Structural Modification on Diazatricyclodecane Derivatives". Molecules 26, № 18 (2021): 5448. http://dx.doi.org/10.3390/molecules26185448.

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Opioid analgesics are clinically used to relieve severe pain in acute postoperative and cancer pain, and also in the long term in chronic pain. The analgesic action is mediated by μ-, δ-, and κ-receptors, but currently, with few exceptions for k-agonists, μ-agonists are the only ones used in therapy. Previously synthesized compounds with diazotricyclodecane cores (DTDs) have shown their effectiveness in binding opioid receptors. Fourteen novel diazatricyclodecanes belonging to the 9-propionyl-10-substituted-9,10-diazatricyclo[4.2.1.12,5]decane (compounds 20–23, 53, 57 and 59) and 2-propionyl-7
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16

Hampson, Robert E., Jian Mu, and Sam A. Deadwyler. "Cannabinoid and Kappa Opioid Receptors Reduce Potassium K Current via Activation of Gs Proteins in Cultured Hippocampal Neurons." Journal of Neurophysiology 84, no. 5 (2000): 2356–64. http://dx.doi.org/10.1152/jn.2000.84.5.2356.

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The current study showed that potassium K current ( I K), which is evoked at depolarizing potentials between −30 and +40 mV in cultured hippocampal neurons, was significantly reduced by exposure to the CB1 cannabinoid receptor agonist WIN 55,212-2 (WIN-2). WIN-2 (20–40 nM) produced an average 45% decrease in I K amplitude across all voltage steps, which was prevented by SR141716A, the CB1 receptor antagonist. The cannabinoid receptor has previously been shown to be Gi/o protein-linked to several cellular processes; however, the decrease in I Kwas unaffected by modulators of Gi/o proteins and a
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17

Madamba, Samuel G., Paul Schweitzer, and George Robert Siggins. "Nociceptin Augments K+ Currents in Hippocampal CA1 Neurons by Both ORL-1 and Opiate Receptor Mechanisms." Journal of Neurophysiology 82, no. 4 (1999): 1776–85. http://dx.doi.org/10.1152/jn.1999.82.4.1776.

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We previously reported (see also the accompanying paper) that dynorphin A significantly enhanced the voltage-dependent K+ M-current ( I M) in CA3 and CA1 hippocampal pyramidal neurons (HPNs). Because the opioid-receptor-like-1 (ORL-1) receptor shares a high sequence homology with opioid receptors and is expressed in rat hippocampus, we examined the effects of orphanin FQ or nociceptin, the endogenous ligand for the ORL-1 receptor, using the rat hippocampal slice preparation and intracellular voltage-clamp recording. Current-voltage ( I-V) relationships from CA1 HPNs revealed that nociceptin su
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18

Ikeda, Yukio, and Yasuhiro Yamamoto. "Effect of selective k-opioid receptor antagonist on traumatic brain edema." Nihon Kyukyu Igakukai Zasshi 10, no. 1 (1999): 28–29. http://dx.doi.org/10.3893/jjaam.10.28.

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19

Deng, Haiping, Zhijie Yang, Yuting Li та ін. "Interactions of Na+,K+-ATPase and co-expressed δ-opioid receptor". Neuroscience Research 65, № 3 (2009): 222–27. http://dx.doi.org/10.1016/j.neures.2009.07.003.

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20

Portoghese, P. S., A. W. Lipkowski, and A. E. Takemori. "Binaltorphimine and nor-binaltorphimine, potent and selective k-opioid receptor antagonists." Life Sciences 40, no. 13 (1987): 1287–92. http://dx.doi.org/10.1016/0024-3205(87)90585-6.

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21

Gopalsamy, Banulata, Jasmine Siew Min Chia, Ahmad Akira Omar Farouk, Mohd Roslan Sulaiman, and Enoch Kumar Perimal. "Zerumbone-Induced Analgesia Modulated via Potassium Channels and Opioid Receptors in Chronic Constriction Injury-Induced Neuropathic Pain." Molecules 25, no. 17 (2020): 3880. http://dx.doi.org/10.3390/molecules25173880.

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Zerumbone, a monocyclic sesquiterpene from the wild ginger plant Zingiber zerumbet (L.) Smith, attenuates allodynia and hyperalgesia. Currently, its mechanisms of action in neuropathic pain conditions remain unclear. This study examines the involvement of potassium channels and opioid receptors in zerumbone-induced analgesia in a chronic constriction injury (CCI) neuropathic pain mice model. Male Institute of Cancer Research (ICR) mice were subjected to CCI and behavioral responses were tested on day 14. Responses toward mechanical allodynia and thermal hyperalgesia were tested with von Frey’s
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22

Hassanian-Moghaddam, H., S. Afzali, and A. Pooya. "Withdrawal syndrome caused by naltrexone in opioid abusers." Human & Experimental Toxicology 33, no. 6 (2013): 561–67. http://dx.doi.org/10.1177/0960327112450901.

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Study objective: Naltrexone is a competitive opioid receptor antagonist acting at the µ- and k-opioid receptors that blocks the euphoric effects of exogenous administered opioids. When used in opioid-dependent patients, naltrexone can cause acute and severe withdrawal symptoms. Methods: This was a cross-sectional study conducted from December 2007 to March 2008 and consisted of patients who had used naltrexone accidentally or deliberately and were referred to Loghman-Hakim Poison Hospital, Tehran, Iran. All symptoms and signs were assessed and the relationship between the dose of naltrexone, o
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23

Yu, Tzu-Ping, and Cui-Wei Xie. "Orphanin FQ/Nociceptin Inhibits Synaptic Transmission and Long-Term Potentiation in Rat Dentate Gyrus Through Postsynaptic Mechanisms." Journal of Neurophysiology 80, no. 3 (1998): 1277–84. http://dx.doi.org/10.1152/jn.1998.80.3.1277.

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Yu, Tzu-Ping and Cui-Wei Xie. Orphanin FQ/nociceptin inhibits synaptic transmission and long-term potentiation in the rat dentate gyrus through postsynaptic mechanisms. J. Neurophysiol. 80: 1277–1284, 1998. Orphanin FQ/nociceptin (OFQ), a recently characterized natural ligand for the opioid receptor-like 1 (ORL1) receptor, shares structural similarity to the endogenous opioids. Our previous study found that OFQ, like classical opioids, modulated synaptic transmission and long-term potentiation (LTP) in the hippocampal CA1 region, suggesting a modulatory role for OFQ in synaptic plasticity invo
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Bhardwaj, Anish, Thomas Jk Toung, Jeffrey R. Kirsch, Raymond C. Koehler, Patricia D. Hurn, and Richard J. Traystman. "NEUROPROTECTIVE EFFECTS OF KAPPA OPIOID RECEPTOR AGONIST IN TRANSIENT FOCAL ISCHEMIA." Stroke 32, suppl_1 (2001): 355. http://dx.doi.org/10.1161/str.32.suppl_1.355-c.

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P91 Kappa ( K ) opioid receptors have been implicated in neuroprotection from ischemic neuronal injury. We tested the effects of a selective and specific K -opioid receptor agonist, BRL 52537 and antagonist, norBNI on infarction volume following transient focal ischemia in the rat. Under controlled conditions of normoxia, normocarbia and normothermia, halothane (1–2%)-anesthetized male Wistar rats (250–300 g) were subjected to 2 hr of middle cerebral artery occlusion (MCAO) by the intraluminal occlusion-technique using laser Doppler perfusion to assess intensity of ischemia. In a blinded rando
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Peart, Jason N., and Garrett J. Gross. "Adenosine and opioid receptor-mediated cardioprotection in the rat: evidence for cross-talk between receptors." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 1 (2003): H81—H89. http://dx.doi.org/10.1152/ajpheart.00985.2002.

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The relative roles of free-radical production, mitochondrial ATP-sensitive K+ (mitoKATP) channels and possible receptor cross-talk in both opioid and adenosine A1 receptor (A1AR) mediated protection were assessed in a rat model of myocardial infarction. Sprague-Dawley rats were subjected to 30 min of occlusion and 90 min of reperfusion. The untreated rats exhibited an infarct of 58.8 ± 2.9% [infarct size (IS)/area at risk (AAR), %] at the end of reperfusion. Pretreatment with either the nonselective opioid receptor agonist morphine or the selective A1AR agonist 2-chloro-cyclopentyladenosine (C
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26

Zakaria, Zainul Amiruddin, Mohammad Hafiz Abdul Rahim, Rushduddin Al Jufri Roosli, et al. "Antinociceptive Activity of Methanolic Extract ofClinacanthus nutansLeaves: Possible Mechanisms of Action Involved." Pain Research and Management 2018 (March 4, 2018): 1–15. http://dx.doi.org/10.1155/2018/9536406.

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Methanolic extract ofClinacanthus nutansLindau leaves (MECN) has been proven to possess antinociceptive activity that works via the opioid and NO-dependent/cGMP-independent pathways. In the present study, we aimed to further determine the possible mechanisms of antinociception of MECN using various nociceptive assays. The antinociceptive activity of MECN was (i) tested against capsaicin-, glutamate-, phorbol 12-myristate 13-acetate-, bradykinin-induced nociception model; (ii) prechallenged against selective antagonist of opioid receptor subtypes (β-funaltrexamine, naltrindole, and nor-binaltor
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Su, Diansan, John Riley, Willis J. Kiessling, William M. Armstead та Renyu Liu. "Salvinorin A Produces Cerebrovasodilation through Activation of Nitric Oxide Synthase, κ Receptor, and Adenosine Triphosphate–sensitive Potassium Channel". Anesthesiology 114, № 2 (2011): 374–79. http://dx.doi.org/10.1097/aln.0b013e318204e029.

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Background Salvinorin A is a nonopioid, selective κ opioid-receptor agonist. Despite its high potential for clinical application, its pharmacologic profile is not well known. In the current study, we hypothesized that salvinorin A dilates pial arteries via activation of nitric oxide synthase, adenosine triphosphate-sensitive potassium channels, and opioid receptors. Methods Cerebral artery diameters and cyclic guanosine monophosphate in cortical periarachnoid cerebrospinal fluid were monitored in piglets equipped with closed cranial windows. Observation took place before and after salvinorin A
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Minami, Masabumi, Takashi Toya, Yoshikazu Katao, et al. "Cloning and expression of a cDNA for the rat k -opioid receptor." FEBS Letters 329, no. 3 (1993): 291–95. http://dx.doi.org/10.1016/0014-5793(93)80240-u.

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Jackson, Helen C., and Ian Kitchen. "Lack of effect of perinatal lead exposure on K-opioid receptor function." Toxicology Letters 50, no. 1 (1990): 17–23. http://dx.doi.org/10.1016/0378-4274(90)90248-k.

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Salman, Shaima, Alison C. Holloway та Colin A. Nurse. "Chronic opioids regulate KATP channel subunit Kir6.2 and carbonic anhydrase I and II expression in rat adrenal chromaffin cells via HIF-2α and protein kinase A". American Journal of Physiology-Cell Physiology 307, № 3 (2014): C266—C277. http://dx.doi.org/10.1152/ajpcell.00135.2014.

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At birth, asphyxial stressors such as hypoxia and hypercapnia are important physiological stimuli for adrenal catecholamine release that is critical for the proper transition to extrauterine life. We recently showed that chronic opioids blunt chemosensitivity of neonatal rat adrenomedullary chromaffin cells (AMCs) to hypoxia and hypercapnia. This blunting was attributable to increased ATP-sensitive K+ (KATP) channel and decreased carbonic anhydrase (CA) I and II expression, respectively, and involved μ- and δ-opioid receptor signaling pathways. To address underlying molecular mechanisms, we fi
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Johnson, S. M., J. C. Smith, and J. L. Feldman. "Modulation of respiratory rhythm in vitro: role of Gi/o protein-mediated mechanisms." Journal of Applied Physiology 80, no. 6 (1996): 2120–33. http://dx.doi.org/10.1152/jappl.1996.80.6.2120.

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Slice preparations from neonatal rat medulla that generate respiratory rhythm in vitro were used to test for Gi/o protein-mediated mechanisms affecting breathing rhythm in mammals. The frequency of inspiratory motor discharge recorded from hypoglossal (XII) nerve roots decreased with bath application of gamma-aminobutyric acid (GABA) and norepinephrine, as well as agonists specific for GABAB, alpha 2-adrenergic, and mu-opioid receptors; 5-hydroxytryptamine had little effect on frequency. Microinjection of these specific agonists into the pre-Botzinger complex, the site of respiratory rhythm ge
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Kanematsu, Ken, and Takeshi Sagara. "An Approach to the Rational Design of Opioid Receptor Ligands Non-narcotic k-Opioid Receptor Ligand KT-95 Free from Euphoria and or Dysphoria." Current Medicinal Chemistry-Central Nervous System Agents 1, no. 1 (2001): 1–25. http://dx.doi.org/10.2174/1568015013358716.

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Kuzume, Koh, Roger A. Wolff, Kazuhiko Amakawa, Kazuyo Kuzume, and Donna M. Van Winkle. "Sustained exogenous administration of Met5-enkephalin protects against infarction in vivo." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (2003): H2463—H2470. http://dx.doi.org/10.1152/ajpheart.00341.2003.

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The opioid antagonist naloxone abolishes infarct limitation by myocardial ischemic preconditioning, suggesting that one or more endogenous opioid peptides can mediate cardiac protection against ischemic damage. We tested the hypothesis that the naturally occurring opioid peptide Met5-enkephalin (ME) modulates myocardial infarct size in vivo. Experiments were conducted in barbiturate-anesthetized open-chest rabbits subjected to regional myocardial ischemia-reperfusion. ME was administered via osmotic minipump for 24 h. Infarct size was assessed with tetrazolium and is expressed as a percentage
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Liu, Sumei, Hong-Zhen Hu, Jun Ren, et al. "Pre- and postsynaptic inhibition by nociceptin in guinea pig small intestinal myenteric plexus in vitro." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 1 (2001): G237—G246. http://dx.doi.org/10.1152/ajpgi.2001.281.1.g237.

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Actions of nociceptin on electrical and synaptic behavior of morphologically and neurochemically identified neurons in the guinea pig duodenal myenteric plexus were studied with conventional techniques. Nociceptin hyperpolarized the membrane potential in 104 of 121 AH-type and 28 of 51 S-type neurons with an EC50 of 11.9 ± 1.2 nM. Increased K+ conductance accounted for the hyperpolarizing responses that were blocked by pertussis toxin and unaffected by naloxone. The selective opioid receptor-like (ORL)1 receptor antagonist [Phe1-psi(CH2-NH)-Gly2]nociceptin(1–13)-NH2suppressed the nociceptin-ev
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Galla, Fabian, Christian Bourgeois, Kirstin Lehmkuhl та ін. "Effects of polar κ receptor agonists designed for the periphery on ATP-induced Ca2+ release from keratinocytes". MedChemComm 7, № 2 (2016): 317–26. http://dx.doi.org/10.1039/c5md00414d.

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The very polar pyridylmethyl derivative 5a (log D<sub>7.4</sub> = 1.1) represents a potent and selective full κ-opioid receptor agonist (K<sub>i</sub> = 0.13 nM, EC<sub>50</sub> = 33 nM), which reduced the release of Ca<sup>2+</sup>-ions into the cytoplasm in human keratinocytes.
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Barber, A., G. D. Bartoszyk, H. M. Bender, et al. "A pharmacological profile of the novel, peripherally-selective k-opioid receptor agonist, EMD 61753." British Journal of Pharmacology 113, no. 4 (1994): 1317–27. http://dx.doi.org/10.1111/j.1476-5381.1994.tb17142.x.

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Ocaña, Maria, Esperanza Pozo, Manuel Barrios та José M. Baeyens. "Subgroups among μ-opioid receptor agonists distinguished by ATP-sensitive K+ channel-acting drugs". British Journal of Pharmacology 114, № 6 (1995): 1296–302. http://dx.doi.org/10.1111/j.1476-5381.1995.tb13346.x.

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38

LEE, H. THOMAS, and CHARLES W. EMALA. "Protein Kinase C and Gi/o Proteins Are Involved in Adenosine- and Ischemic Preconditioning—Mediated Renal Protection." Journal of the American Society of Nephrology 12, no. 2 (2001): 233–40. http://dx.doi.org/10.1681/asn.v122233.

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Abstract. Renal ischemic reperfusion (IR) injury is a significant clinical problem in anesthesia and surgery. Recently, it was demonstrated that both renal ischemic preconditioning (IPC) and systemic adenosine pretreatment protect against renal IR injury. In cardiac IPC, pertussis toxin-sensitive G-proteins (i.e., Gi/o), protein kinase C (PKC), and ATP-sensitive potassium (K+ATP) channels are implicated in this protective signaling pathway. The aim of this study was to elucidate the signaling pathways that are responsible for renal protection mediated by both IPC and adenosine pretreatment. In
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39

Hansson, E., L. Block, U. Björklund, and B. Biber. "Inflammation-reactive astrocytes can be restored with a three drug combination." Scandinavian Journal of Pain 5, no. 3 (2014): 209. http://dx.doi.org/10.1016/j.sjpain.2014.05.016.

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Abstract Aims In inflammation-reactive astrocytes the cell parameters, Ca2+ signalling, Na+ transporters, cytoskeleton, and release of proinflammatory cytokines are affected. We want to re-establish these parameters with agents, which might have a potential to restore the cells back to a normal non-inflammatory level. Methods Astrocytes in primary cultures were incubated with lipopolysaccharide (LPS) (10 ng/ml) for 24 h to become inflammation-reactive. Different parameters were analysed to verify this inflammation: Ca2+ signalling, Na+/K+-ATPase expression, actin filament organization, and int
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Ronsisvalle, Giuseppe, Agostino Marrazzo, Orazio Prezzavento, et al. "Opioid and sigma receptor studies. New developments in the design of selective sigma ligands." Pure and Applied Chemistry 73, no. 9 (2001): 1499–509. http://dx.doi.org/10.1351/pac200173091499.

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New racemic and chiral methyl 2-{[4-(4-chlorophenyl)-4-hydroxypiperi-din-1-yl]methyl}-1-phenylcyclopropanecarboxylate derivatives were synthesized in order to obtain sigma ligands with increased affinity and selectivity compared to (+)-MPCB and haloperidol. The cis-(±)-7 racemic mixture showed a better binding affinity and selectivity than the (±)-8 trans isomers. Between the two cis enantiomers, (+)-7, with configuration (1R,2S), showed a very high affinity and the best selectivity for s1. All compounds synthesized (7­9) showed a reduced or negligible affinity for opioid and dopaminergic D1 a
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Williams, Wynford R. "Dampening of neurotransmitter action: molecular similarity within the melatonin structure." Endocrine Regulations 52, no. 4 (2018): 199–207. http://dx.doi.org/10.2478/enr-2018-0025.

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AbstractObjectives. Melatonin initiates physiologic and therapeutic responses in various tissues through binding to poorly defined MT receptors regulated by G-proteins and purine nucleotides. Melatonin’s interaction with other G-protein regulated receptors, including those of serotonin, is unclear. This study explores the potential for the interaction of melatonin with nucleotide and receptor ligand structures. Methods. The study uses a computational program to investigate relative molecular similarity by the comparative superimposition and quantitative fitting of molecular structures to adeni
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Shinmura, Ken, Maiko Nagai, Kayoko Tamaki, Masato Tani, and Roberto Bolli. "COX-2-derived prostacyclin mediates opioid-induced late phase of preconditioning in isolated rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (2002): H2534—H2543. http://dx.doi.org/10.1152/ajpheart.00209.2002.

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Opioids confer biphasic (early and late) cardioprotection against myocardial infarction by opening mitochondrial ATP-sensitive K+ channels. It is unknown whether cyclooxygenase-2 (COX-2), which mediates ischemia-induced late preconditioning, also mediates opioid-induced cardioprotection. Isolated perfused rat hearts were subjected to 20 min of global ischemia followed by 20 min of reperfusion. BW-373U86 (BW), a δ-opioid receptor agonist, was administered 1, 12, or 24 h before death. Recovery of left ventricular developed pressure (LVDP) after ischemia-reperfusion improved when BW was administe
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Godínez-Chaparro, Beatriz, Fabiola Guzmán-Mejía, and Maria Elisa Drago-Serrano. "Lactoferrin and Its Potential Impact for the Relief of Pain: A Preclinical Approach." Pharmaceuticals 14, no. 9 (2021): 868. http://dx.doi.org/10.3390/ph14090868.

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Pain is one of the most disabling symptoms of several clinical conditions. Neurobiologically, it is classified as nociceptive, inflammatory, neuropathic and dysfunctional. Opioids and nonsteroidal anti-inflammatory drugs (NSAIDs) are conventionally prescribed for the treatment of pain. Long-term administration of opioids results in the loss of analgesic efficacy, leading to increased dosage, tolerance, and addiction as the main drawbacks of their use, while the adverse effects of NSAIDs include gastric ulcer formation, intestinal bleeding, acute kidney injury, and hepatotoxicity. Lactoferrin i
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Ortiz, Mario I., Raquel Cariño-Cortés, and Gilberto Castañeda-Hernández. "Participation of the opioid receptor – nitric oxide – cGMP – K+ channel pathway in the peripheral antinociceptive effect of nalbuphine and buprenorphine in rats." Canadian Journal of Physiology and Pharmacology 98, no. 11 (2020): 753–62. http://dx.doi.org/10.1139/cjpp-2020-0104.

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The aim of this study was to examine if the peripheral antinociceptive effects of the opioid agonist/antagonist nalbuphine and buprenorphine involve the sequential participation of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) synthesis followed by K+ channel opening in the formalin test. Wistar rats (180–220 g) were injected in the dorsal surface of the right hind paw with formalin (1%). Rats received a subcutaneous (s.c.) injection into the dorsal surface of the paw of vehicles or increasing doses of nalbuphine (50–200 μg/paw) or buprenorphine (1–5 μg/paw) 20 min before formali
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Furuya, Yoshiaki, Takahiro Nakazawa, Takeru Kaneko, and Kiyomi Yamatsu. "Evidence for the involvement of the spinal k-opioid receptor in E-2078-induced analgesia." Japanese Journal of Pharmacology 49 (1989): 237. http://dx.doi.org/10.1016/s0021-5198(19)56546-5.

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46

Wadenberg, M.-L. G. "A Review of the Properties of Spiradoline: A Potent and Selective k-Opioid Receptor Agonist." CNS Drug Reviews 9, no. 2 (2006): 187–98. http://dx.doi.org/10.1111/j.1527-3458.2003.tb00248.x.

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Ortiz, Mario I., Jhanet Castro-Olguín, Nayeli Peña-Samaniego, and Gilberto Castañeda-Hernández. "Probable activation of the opioid receptor-nitric oxide-cyclic GMP-K+ channels pathway by codeine." Pharmacology Biochemistry and Behavior 82, no. 4 (2005): 695–703. http://dx.doi.org/10.1016/j.pbb.2005.11.011.

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48

Cilia, Roberto, Rosanna Asselta, Emanuele Cereda, et al. "Opioid K receptor variant is associated with a delayed onset of dyskinesias in Parkinson’s disease." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 3 (2017): 323–24. http://dx.doi.org/10.1136/jnnp-2017-316235.

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49

Masocha, Willias, Luis G. González та Ahmad Agil. "Distinguishing subgroups among μ-opioid receptor agonists using Na+,K+-ATPase as an effector mechanism". European Journal of Pharmacology 774 (березень 2016): 43–49. http://dx.doi.org/10.1016/j.ejphar.2016.01.010.

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Pacheco, Daniela F., та Igor D. G. Duarte. "δ-Opioid receptor agonist SNC80 induces peripheral antinociception via activation of ATP-sensitive K+ channels". European Journal of Pharmacology 512, № 1 (2005): 23–28. http://dx.doi.org/10.1016/j.ejphar.2005.02.018.

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