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Journal articles on the topic 'Ethanol Ethanol Opioid peptides'

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Published: 4 June 2021

Last updated: 2 February 2022

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1

Goldberg, Joel S. "Low Molecular Weight Opioid Peptide Esters Could be Developed as a New Class of Analgesics." Perspectives in Medicinal Chemistry 5 (January 2011): PMC.S6803. http://dx.doi.org/10.4137/pmc.s6803.

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Low molecular weight opioid peptide esters (OPE) could become a class of analgesics with different side effect profiles than current opiates. OPE may have sufficient plasma stability to cross the blood brain barrier (BBB), undergo ester hydrolysis and produce analgesia. OPE of dipeptides, tyr-pro and tyr-gly conjugated to ethanol have a structure similar to the anesthestic agent, etomidate. Based upon the analgesic activity of dipeptide opioids, Lipinski's criteria, and permeability of select GABA esters to cross the BBB, opioid peptides (OP) conjugated to ethanol, cholesterol or 3-glucose are lead recommendations. Preliminary animal data suggests that tyr-pro-ethyl ester crosses the BBB and unexpectedly produces hyperalgesia. Currently, there are no approved OP analgesics available for clinical use. Clinical trials of good manufacturing practice OP administered to patients suffering from chronic pain with indwelling intrathecal pumps could resolve the issue that OP may be superior to opiates and may redirect research.

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2

Coiro, V., A. Alboni, D. Gramellini, C. Cigarini, L. Bianconi, D. Pignatti, R. Volpi, and P. Chiodera. "Inhibition by ethanol of the oxytocin response to breast stimulation in normal women and the role of endogenous opioids." Acta Endocrinologica 126, no. 3 (March 1992): 213–16. http://dx.doi.org/10.1530/acta.0.1260213.

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The possible inhibition exerted by ethanol on the oxytocin response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the oxytocin response to breast stimulation and/or ethanol action was also examined. Sixteen normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 or 4 mg in an iv bolus plus 5 or 10 mg over 16 min), ethanol (50 ml in 110ml of whisky po) or the combination of ethanol and naloxone. Plasma oxytocin levels rose about twofold after breast stimulation, with a mean peak response at 10 min. The oxytocin response to breast stimulation was not changed by the treatment with the lower (2 plus 5 mg) or the higher (4 plus 10 mg) dose of naloxone, whereas it was completely abolished by ethanol. However, when ethanol was given together with naloxone, the oxytocin rise induced by breast stimulation was only partially inhibited by ethanol (the mean oxytocin peak was 50% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the oxytocin response to breast stimulation. Naloxone sensitive endogenous opioids do not appear to be involved in the control of the oxytocin rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

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3

Gianoulakis, C. "The effect of ethanol on the biosynthesis and regulation of opioid peptides." Experientia 45, no. 5 (May 1989): 428–35. http://dx.doi.org/10.1007/bf01952024.

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4

Chang, Guo-Qing, Olga Karatayev, Rashedul Ahsan, Nicole M. Avena, Caroline Lee, Michael J. Lewis, Bartley G. Hoebel, and Sarah F. Leibowitz. "Effect of Ethanol on Hypothalamic Opioid Peptides, Enkephalin, and Dynorphin: Relationship With Circulating Triglycerides." Alcoholism: Clinical and Experimental Research 31, no. 2 (February 2007): 249–59. http://dx.doi.org/10.1111/j.1530-0277.2006.00312.x.

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5

Przewłocka, Barbara, Wiadysław Lasoń, and Ryszard Przewłocki. "Repeated Ethanol Differently Affects Opioid Peptide Biosynthesis in the Rat Pituitary." Neuroendocrinology 60, no. 3 (1994): 331–36. http://dx.doi.org/10.1159/000126766.

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6

Palm, Sara, Erika Roman, and Ingrid Nylander. "Differences in basal and ethanol-induced levels of opioid peptides in Wistar rats from five different suppliers." Peptides 36, no. 1 (July 2012): 1–8. http://dx.doi.org/10.1016/j.peptides.2012.04.016.

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7

Gustafsson, L., Q. Zhou, and I. Nylander. "Ethanol-induced effects on opioid peptides in adult male Wistar rats are dependent on early environmental factors." Neuroscience 146, no. 3 (May 2007): 1137–49. http://dx.doi.org/10.1016/j.neuroscience.2007.02.037.

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8

Boyadjieva, Nadka, Madhavi Dokur, Juan P. Advis, Gary G. Meadows, and Dipak K. Sarkar. "Chronic Ethanol Inhibits NK Cell Cytolytic Activity: Role of Opioid Peptide β-Endorphin." Journal of Immunology 167, no. 10 (November 15, 2001): 5645–52. http://dx.doi.org/10.4049/jimmunol.167.10.5645.

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9

Jarjour, Samuel, Li Bai, and Christina Gianoulakis. "Effect of Acute Ethanol Administration on the Release of Opioid Peptides From the Midbrain Including the Ventral Tegmental Area." Alcoholism: Clinical and Experimental Research 33, no. 6 (June 2009): 1033–43. http://dx.doi.org/10.1111/j.1530-0277.2009.00924.x.

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10

Przewo̵cka, B., W. Lasoń, and R. Przewlocki. "Effect of repeated ethanol administration on opioid peptide systems activity in rat hypothalamus and pituitary." Pharmacological Research 25 (May 1992): 71–72. http://dx.doi.org/10.1016/1043-6618(92)90292-j.

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11

Ploj, Karolina, Erika Roman, Ants Kask, Petri Hyytiä, Helgi B. Schiöth, Jarl E. S. Wikberg, and Ingrid Nylander. "Effects of melanocortin receptor ligands on ethanol intake and opioid peptide levels in alcohol-preferring AA rats." Brain Research Bulletin 59, no. 2 (October 2002): 97–104. http://dx.doi.org/10.1016/s0361-9230(02)00844-4.

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12

Lam, Minh P., Peter W. Marinelli, Li Bai, and Christina Gianoulakis. "Effects of acute ethanol on opioid peptide release in the central amygdala: an in vivo microdialysis study." Psychopharmacology 201, no. 2 (August 8, 2008): 261–71. http://dx.doi.org/10.1007/s00213-008-1267-8.

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13

Rapaka, Rao S., Venkatesan Renugopalakrishnan, Thomas J. Goehl, and Bradley J. Collins. "Ethanol induced conformational changes of the peptide ligands for the opioid receptors and their relevance to receptor interaction." Life Sciences 39, no. 9 (September 1986): 837–42. http://dx.doi.org/10.1016/0024-3205(86)90463-7.

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14

Caputi, Francesca Felicia, Serena Stopponi, Laura Rullo, Martina Palmisano, Massimo Ubaldi, Sanzio Candeletti, Roberto Ciccocioppo, and Patrizia Romualdi. "Dysregulation of Nociceptin/Orphanin FQ and Dynorphin Systems in the Extended Amygdala of Alcohol Preferring Marchigian Sardinian (msP) Rats." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2448. http://dx.doi.org/10.3390/ijms22052448.

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Previous studies have shown that genetically selected Marchigian Sardinian alcohol-preferring (msP) rats consume excessive amounts of ethanol to self-medicate from negative moods and to relieve innate hypersensitivity to stress. This phenotype resembling a subset of alcohol use disorder (AUD) patients, appears to be linked to a dysregulation of the equilibrium between stress and antistress mechanisms in the extended amygdala. Here, comparing water and alcohol exposed msP and Wistar rats we evaluate the transcript expression of the anti-stress opioid-like peptide nociceptin/orphanin FQ (N/OFQ) and its receptor NOP as well as of dynorphin (DYN) and its cognate κ-opioid receptor (KOP). In addition, we measured the transcript levels of corticotropin-releasing factor (CRF), CRF receptor 1 (CRF1R), brain-derived neurotrophic factor (BDNF) and of the tropomyosin receptor kinase B receptor (Trk-B). Results showed an innately up-regulation of the CRFergic system, mediating negative mood and stress responses, as well as an inherent up-regulation of the anti-stress N/OFQ system, both in the amygdala (AMY) and bed nucleus of the stria terminalis (BNST) of msP rats. The up-regulation of this latter system may reflect an attempt to buffer the negative condition elicited by the hyperactivity of pro-stress mechanisms since results showed that voluntary alcohol consumption dampened N/OFQ. Alcohol exposure also reduced the expression of dynorphin and CRF transmissions in the AMY of msP rats. In the BNST, alcohol intake led to a more complex reorganization of these systems increasing receptor transcripts in msP rats, along with an increase of CRF and a decrease of N/OFQ transcripts, respectively. Moreover, mimicking the effects of alcohol in the AMY we observed that the activation of NOP receptor by intracerebroventricular administration of N/OFQ in msP rats caused an increase of BDNF and a decrease of CRF transcripts. Our study indicates that both stress and anti-stress mechanisms are dysregulated in the extended AMY of msP rats. The voluntary alcohol drinking, as well as NOP agonism, have a significant impact on neuropeptidergic systems arrangement, bringing the systems back to normalization.

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15

Froehlich, Janice C., and Gary Wand. "The Neurobiology of Ethanol-Opioid Interactions in Ethanol Reinforcement." Alcoholism: Clinical and Experimental Research 20, s8 (November 1996): 181a—186a. http://dx.doi.org/10.1111/j.1530-0277.1996.tb01772.x.

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16

Charness, M. E. "Ethanol and opioid receptor signalling." Experientia 45, no. 5 (May 1989): 418–28. http://dx.doi.org/10.1007/bf01952023.

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17

Roberts, A. J., S. Ghozland, C. Chu, and C. Kincaid. "THE MU OPIOID RECEPTOR MODULATES ACUTE ETHANOL SENSITIVITY AND ETHANOL WITHDRAWAL SEVERITY." Alcoholism: Clinical & Experimental Research 28, Supplement (August 2004): 86A. http://dx.doi.org/10.1097/00000374-200408002-00475.

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18

Wilkemeyer, Michael F., Shao-yu Chen, Carrie E. Menkari, Kathleen K. Sulik, and Michael E. Charness. "Ethanol Antagonist Peptides: Structural Specificity without Stereospecificity." Journal of Pharmacology and Experimental Therapeutics 309, no. 3 (February 4, 2004): 1183–89. http://dx.doi.org/10.1124/jpet.103.063818.

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19

Arias, Carlos, and M. Gabriela Chotro. "Increased palatability of ethanol after prenatal ethanol exposure is mediated by the opioid system." Pharmacology Biochemistry and Behavior 82, no. 3 (November 2005): 434–42. http://dx.doi.org/10.1016/j.pbb.2005.09.015.

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20

Golovko, A. I. "Amethystic agents influencing toxicodynamics of ethanol." Biomeditsinskaya Khimiya 59, no. 6 (2013): 604–21. http://dx.doi.org/10.18097/pbmc20135906604.

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The pathogenetic mechanisms of acute alcoholic intoxications are examined and is based the expediency of the search for the amethystic agents, which influence neurotransmitter systems. Promising should be considered the agents, which modulate GABA-systems (partial reverse agonists of benzodiazepine receptors), glutamate (antagonists of metabotropic receptors mGluR2/3), opioid neuropeptides (antagonists of opioid receptors), acetylcholine (reversible inhibitors of acetylcholinesterase and M-cholinoagonists), adenosine (selective antagonists of A -receptors). The amethystic effect manifest also the substances, which modify the second messengers systems (calcium, nitrergic and cascade of arachidonic acid). The most of the means examined possesses the moderate amethystic potential, and effectiveness is manifested predominantly during the preventive application.

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21

Gomes, Ivone, Nino Trapaidze, Herman Turndorf, Lakshmi Arehole Devi, and Mylarrao Bansinath. "Acute Ethanol Treatment Modulates δ Opioid Receptors in N18TG2 Cells." Anesthesiology 92, no. 6 (June 1, 2000): 1789–98. http://dx.doi.org/10.1097/00000542-200006000-00039.

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Background The in vitro adaptive responses of delta opiate receptors (DOR) to chronic ethanol treatment have been well documented. The acute effects of ethanol on these receptors are not well characterized beyond its effect on ligand binding. The aim of this study was to evaluate the acute effects of clinically relevant concentrations of ethanol (50-200 mm) on the saturation binding kinetics, receptor/ligand internalization, and agonist stimulation of G-protein coupling in N18TG2 cells expressing the Flag epitope-tagged mouse DOR. Methods Confocal microscopy was used to localize Flag epitope-tagged DOR in N18TG2 cells. Saturation binding assays at 4 degrees C and 37 degrees C were conducted in the absence or presence of ethanol on cells not pretreated or pretreated with ethanol for 30 min at 37 degrees C. Highly specific delta agonist, DPDPE ([D-Pen2,D-Pen5]enkephalin), was used in these studies. The effect of ethanol on agonist stimulation of G-protein coupling was examined using [35S]GTPgammaS (guanosine-5'-O-(3-thio)triphosphate) binding to membranes. Agonist-mediated receptor internalization was examined using flow cytometry of cells labeled with the antiserum directed against the Flag epitope, and the ligand internalization was examined using [3H]DPDPE. Results Ethanol decreased the binding of the agonist [3H]DPDPE, and not the antagonist [3H]diprenorphine, in a dose-dependent manner. These effects were temperature-dependent. Ethanol reversibly inhibited agonist stimulation of [35S]GTPgammaS binding. In non-pretreated cells, ethanol decreased the rate of receptor/ligand internalization, but this effect was not seen in ethanol pretreated cells. Taken together, these results suggest that pretreatment of N18TG2 cells with ethanol induces compensatory mechanisms that allow the receptor to function efficiently in its presence. Conclusion Acute ethanol decreased the binding, agonist-mediated functional coupling and receptor/ligand internalization in N18TG2 cells expressing epitope-tagged DOR. In these cells, 30-min pretreatment with ethanol was sufficient to reverse these effects.

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22

Aragon, C. M. G., L.-E. Trudeau, and Z. Amit. "Stress-ethanol interaction: Involvement of endogenous opioid mechanisms." Neuroscience & Biobehavioral Reviews 14, no. 4 (December 1990): 535–41. http://dx.doi.org/10.1016/s0149-7634(05)80080-6.

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23

Coonfield, Daniel L., Stephen W. Kiefer, Frank M. Ferraro, and John David Sinclair. "Ethanol Palatability and Consumption by High Ethanol-Drinking Rats: Manipulation of the Opioid System With Naltrexone." Behavioral Neuroscience 118, no. 5 (2004): 1089–96. http://dx.doi.org/10.1037/0735-7044.118.5.1089.

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24

Mhatre, Molina, and Frank Holloway. "μ1-opioid antagonist naloxonazine alters ethanol discrimination and consumption." Alcohol 29, no. 2 (February 2003): 109–16. http://dx.doi.org/10.1016/s0741-8329(03)00021-1.

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25

Bodd, Egil. "PHARMACOKINETIC INTERACTION BETWEEN SUBSTANCES WITH OPIOID EFFECTS AND ETHANOL." Pharmacology & Toxicology 60 (March 1987): 1–40. http://dx.doi.org/10.1111/j.1600-0773.1987.tb01596.x.

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26

Roberts, Amanda J., Lisa H. Gold, Ilham Polis, Jeffrey S. McDonald, Dominique Filliol, Brigitte L. Kieffer, and George F. Koob. "Increased Ethanol Self-Administration in ??-Opioid Receptor Knockout Mice." Alcoholism: Clinical and Experimental Research 25, no. 9 (September 2001): 1249–56. http://dx.doi.org/10.1097/00000374-200109000-00002.

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27

Kiianmaa, K. "THE ROLE OF OPIOID SYSTEMS IN ETHANOL SELF-ADMINISTRATION." Alcoholism: Clinical & Experimental Research 28, Supplement (August 2004): 77A. http://dx.doi.org/10.1097/00000374-200408002-00425.

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28

Fabio, María Carolina, Ana Fabiola Macchione, Michael E. Nizhnikov, and Ricardo Marcos Pautassi. "Prenatal ethanol increases ethanol intake throughout adolescence, alters ethanol-mediated aversive learning, and affects μ but not δ or κ opioid receptor mRNA expression." European Journal of Neuroscience 41, no. 12 (May 13, 2015): 1569–79. http://dx.doi.org/10.1111/ejn.12913.

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29

Karatayev, Olga, Jessica Baylan, Valerie Weed, Siyi Chang, David Wynick, and Sarah F. Leibowitz. "Galanin Knockout Mice Show Disturbances in Ethanol Consumption and Expression of Hypothalamic Peptides That Stimulate Ethanol Intake." Alcoholism: Clinical and Experimental Research 34, no. 1 (January 2010): 72–80. http://dx.doi.org/10.1111/j.1530-0277.2009.01068.x.

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30

Karatayev, Olga, Jessica R. Barson, Ambrose J. Carr, Jessica Baylan, Yu-Wei Chen, and Sarah F. Leibowitz. "Predictors of ethanol consumption in adult Sprague–Dawley rats: relation to hypothalamic peptides that stimulate ethanol intake." Alcohol 44, no. 4 (June 2010): 323–34. http://dx.doi.org/10.1016/j.alcohol.2010.05.002.

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31

Ikeda, K. "Involvement of GIRK channels in opioid- and ethanol-induced analgesia." Neuroscience Research 38 (2000): S46. http://dx.doi.org/10.1016/s0168-0102(00)81122-0.

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32

Roberts, Amanda J., Lisa H. Gold, Ilham Polis, Jeffrey S. McDonald, Dominique Filliol, Brigitte L. Kieffer, and George F. Koob. "Increased Ethanol Self-Administration in delta-Opioid Receptor Knockout Mice." Alcoholism: Clinical and Experimental Research 25, no. 9 (September 2001): 1249–56. http://dx.doi.org/10.1111/j.1530-0277.2001.tb02344.x.

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33

Xiao, Cheng, Jingli Zhang, Krešimir Krnjević, and Jiang Hong Ye. "Effects of Ethanol on Midbrain Neurons: Role of Opioid Receptors." Alcoholism: Clinical and Experimental Research 31, no. 7 (July 2007): 1106–13. http://dx.doi.org/10.1111/j.1530-0277.2007.00405.x.

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34

Kang-Park, Maeng-Hee, Brigitte L. Kieffer, Amanda J. Roberts, George Robert Siggins, and Scott D. Moore. "Presynaptic δ Opioid Receptors Regulate Ethanol Actions in Central Amygdala." Journal of Pharmacology and Experimental Therapeutics 320, no. 2 (November 17, 2006): 917–25. http://dx.doi.org/10.1124/jpet.106.112722.

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35

Gianoulakis, Christina, Jean-Pascal de Waele, and Joseph Thavundayil. "Implication of the endogenous opioid system in excessive ethanol consumption." Alcohol 13, no. 1 (January 1996): 19–23. http://dx.doi.org/10.1016/0741-8329(95)02035-7.

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36

Harshberger, Erin, Emily A. Gilson, Kelli Gillett, Jasmine H. Stone, Laila El Amrani, and Glenn R. Valdez. "nor-BNI Antagonism of Kappa Opioid Agonist-Induced Reinstatement of Ethanol-Seeking Behavior." Journal of Addiction 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1084235.

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Recent work suggests that the dynorphin (DYN)/kappa opioid receptor (KOR) system may be a key mediator in the behavioral effects of alcohol. The objective of the present study was to examine the ability of the KOR antagonist norbinaltorphimine (nor-BNI) to attenuate relapse to ethanol seeking due to priming injections of the KOR agonist U50,488 at time points consistent with KOR selectivity. Male Wistar rats were trained to self-administer a 10% ethanol solution, and then responding was extinguished. Following extinction, rats were injected with U50,488 (0.1–10 mg/kg, i.p.) or saline and were tested for the reinstatement of ethanol seeking. Next, the ability of the nonselective opioid receptor antagonist naltrexone (0 or 3.0 mg/kg, s.c.) and nor-BNI (0 or 20.0 mg/kg, i.p.) to block U50,488-induced reinstatement was examined. Priming injections U50,488 reinstated responding on the previously ethanol-associated lever. Pretreatment with naltrexone reduced the reinstatement of ethanol-seeking behavior. nor-BNI also attenuated KOR agonist-induced reinstatement, but to a lesser extent than naltrexone, when injected 24 hours prior to injections of U50,488, a time point that is consistent with KOR selectivity. While these results suggest that activation of KORs is a key mechanism in the regulation of ethanol-seeking behavior, U50,488-induced reinstatement may not be fully selective for KORs.

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37

van der Schrier, Rutger, Margot Roozekrans, Erik Olofsen, Leon Aarts, Monique van Velzen, Merijn de Jong, Albert Dahan, and Marieke Niesters. "Influence of Ethanol on Oxycodone-induced Respiratory Depression." Anesthesiology 126, no. 3 (March 1, 2017): 534–42. http://dx.doi.org/10.1097/aln.0000000000001505.

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Abstract Background Respiratory depression is a potentially fatal complication of opioid use, which may be exacerbated by simultaneous ethanol intake. In this three-way sequential crossover dose-escalating study, the influence of coadministration of oral oxycodone and intravenous ethanol was assessed on resting ventilation, apneic events and the hypercapnic ventilatory response in healthy young and older volunteers. Methods Twelve young (21 to 28 yr) and 12 elderly (66 to 77 yr) opioid-naive participants ingested one 20 mg oxycodone tablet combined with an intravenous infusion of 0, 0.5, or 1 g/l ethanol. Resting respiratory variables and the primary outcome, minute ventilation at isohypercapnia (end-tidal partial pressure of carbon dioxide of 55 mmHg or VE55), were obtained at regular intervals during treatment. Results Oxycodone reduced baseline minute ventilation by 28% (P < 0.001 vs. control). Ethanol caused a further decrease of oxycodone-induced respiratory depression by another 19% at 1 g/l ethanol plus oxycodone (P < 0.01 vs. oxycodone). Ethanol combined with oxycodone caused a significant increase in the number of apneic events measured in a 6-min window with a median (range) increase from 1 (0 to 3) at 0 g/l ethanol to 1 (0 to 11) at 1 g/l ethanol (P < 0.01). Mean (95% CI) VE55 decreased from 33.4 (27.9 to 39.0) l/min (control) to 18.6 (15.6 to 21.6) l/min (oxycodone, P < 0.01 vs. control) and to 15.7 (12.7 to 18.6) l/min (oxycodone combined with ethanol, 1 g/l; P < 0.01 vs. oxycodone). Conclusions Ethanol together with oxycodone causes greater ventilatory depression than either alone, the magnitude of which is clinically relevant. Elderly participants were more affected than younger volunteers.

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38

Valdez, Glenn R., and Erin Harshberger. "Kappa opioid regulation of anxiety-like behavior during acute ethanol withdrawal." Pharmacology Biochemistry and Behavior 102, no. 1 (July 2012): 44–47. http://dx.doi.org/10.1016/j.pbb.2012.03.019.

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39

Pautassi, Ricardo Marcos, Michael E. Nizhnikov, Ma Belén Acevedo, and Norman E. Spear. "Early role of the κ opioid receptor in ethanol-induced reinforcement." Physiology & Behavior 105, no. 5 (March 2012): 1231–41. http://dx.doi.org/10.1016/j.physbeh.2012.01.003.

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40

June, Harry L., Collette Grey, Connease Warren-Reese, La Franze Durr, Anila Ricks-Cord, Amanda Johnson, Shannan McCane, et al. "The Opioid Receptor Antagonist Nalmefene Reduces Responding Maintained by Ethanol Presentation." Alcoholism: Clinical & Experimental Research 22, no. 9 (December 1998): 2174. http://dx.doi.org/10.1097/00000374-199812000-00038.

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41

Trigub, M. M., N. G. Bogdanova, A. A. Kolpakov, V. G. Bashkatova, and S. K. Sudakov. "Effect of Peripheral Opioid Receptor Agonists on Depressive Activity of Ethanol." Bulletin of Experimental Biology and Medicine 156, no. 6 (April 2014): 778–80. http://dx.doi.org/10.1007/s10517-014-2448-6.

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42

Cutter, Henry S. G., and Timothy J. O'Farrell. "Experience with alcohol and the endogenous opioid system in ethanol analgesia." Addictive Behaviors 12, no. 4 (January 1987): 331–43. http://dx.doi.org/10.1016/0306-4603(87)90047-5.

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43

Logrip, Marian L., Patricia H. Janak, and Dorit Ron. "Blockade of ethanol reward by the kappa opioid receptor agonist U50,488H." Alcohol 43, no. 5 (August 2009): 359–65. http://dx.doi.org/10.1016/j.alcohol.2009.05.001.

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44

van Rijn, Richard M., Daniela I. Brissett, and Jennifer L. Whistler. "Emergence of Functional Spinal Delta Opioid Receptors After Chronic Ethanol Exposure." Biological Psychiatry 71, no. 3 (February 2012): 232–38. http://dx.doi.org/10.1016/j.biopsych.2011.07.015.

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45

Arias, Carlos, Juan Carlos Molina, and Norman E. Spear. "Differential role of mu, delta and kappa opioid receptors in ethanol-mediated locomotor activation and ethanol intake in preweanling rats." Physiology & Behavior 99, no. 3 (March 2010): 348–54. http://dx.doi.org/10.1016/j.physbeh.2009.11.012.

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46

Wille-Bille, Aranza, Fabio Bellia, Ana María Jiménez García, Roberto Sebastián Miranda-Morales, Claudio D'Addario, and Ricardo Marcos Pautassi. "Early exposure to environmental enrichment modulates the effects of prenatal ethanol exposure upon opioid gene expression and adolescent ethanol intake." Neuropharmacology 165 (March 2020): 107917. http://dx.doi.org/10.1016/j.neuropharm.2019.107917.

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47

June, Harry L., Collette Grey, Connease Warren-Reese, La Franze Durr, Anila Ricks-Cord, Amanda Johnson, Shannan McCane, et al. "The Opioid Receptor Antagonist Nalmefene Reduces Responding Maintained by Ethanol Presentation: Preclinical Studies in Ethanol-Preferring and Outbred Wistar Rats." Alcoholism: Clinical and Experimental Research 22, no. 9 (December 1998): 2174–85. http://dx.doi.org/10.1111/j.1530-0277.1998.tb05931.x.

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Fu, Rao, Xing Chen, Wanhong Zuo, Jing Li, Seungwoo Kang, Li-Hua Zhou, Allan Siegel, Alex Bekker, and Jiang-Hong Ye. "Ablation of μ opioid receptor-expressing GABA neurons in rostromedial tegmental nucleus increases ethanol consumption and regulates ethanol-related behaviors." Neuropharmacology 107 (August 2016): 58–67. http://dx.doi.org/10.1016/j.neuropharm.2016.02.027.

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Sama, Venkatesh, Azmathunnisa Begum, Rajesh Bolleddu, Ravi Alvala, and Jaya Prakash D. "Mechanistic Evaluation of Antinociceptive Effects of Bioactive Guided Fractions of Barleria prionitis." International Journal of Pharmaceutical Sciences and Nanotechnology 10, no. 3 (May 31, 2017): 3715–27. http://dx.doi.org/10.37285/ijpsn.2017.10.3.3.

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Abstract:

Barleria prionitis Linn.(Acanthaceae) is a prickly shrub and traditionally whole plant is used as anti-inflammatory, expectorant, analgesic, diuretic, antirheumaticand antidiabetic. This study was conducted to investigate the antinociceptive and CNS depressant activity of ethanolic extract and the fractions of B. prionitis in mice. Ethanol extract and its fractions were tested at a dose of 200 and 400 mg/kg. Ethanol, petroleum ether and chloroform fractions demonstrated significant antinociceptive activity at 400 mg/kg and significantly increased the latency in hot plate test and the action was antagonised by naloxone, indicating a potential opioid-like mechanism. In conclusion, the ethanol, pet ether and chloroform fractions of B. prionitis markedly demonstrated the antinociceptive action. The CNS depressant and good protective effect on pain stimuli suggest that the possible mechanisms appear to be due to involvement of opioid and/or peripheral receptors.

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Changhao Wu and J. A. Henry. "Interaction between Ethanol and Opioids in a Protozoan Assay." Human & Experimental Toxicology 13, no. 3 (March 1994): 145–48. http://dx.doi.org/10.1177/096032719401300301.

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Abstract:

Ethanol excess combined with opioids can be fatal due to their toxic interaction, yet the nature of the interaction is little documented. Since ethanol and some opioids have membrane stabilizing activity, the present study used a protozoan motility model to test the possibility that ethanol may interact with some opioids on this basis. The EC50 in motility reduction for ethanol, dextropropoxyphene, methadone and pethidine was 522.0± 36.7 mM, 0.59± 0.08 mM, 0.40± 0.09 mM and 4.57± 0.36 mM, respectively. When ethanol was combined with one of the three drugs in equitoxic doses at a ratio of 0.5:0.5, the predicted/observed EC50 values for ethanol-dextropropoxyphene, ethanol-methadone and ethanol-pethidine were 1.37, 1,11 and 1.00, each being close to unity, indicating an additive interaction. The interaction between ethanol and dextropropoxyphene was further explored at 0.25:0.75 and 0.75:0.25 equitoxic dose ratios, with the predicted/observed EC50 values of 0.98 and 0.97, also showing an additive interaction. This suggests that a non-specific interaction between ethanol and opioids may also take place in vivo, which could cause increased toxicity over and above the involvement of opioid receptors, Information from this study should aid understanding of the mechanism of interactions in human poisoning by agents with membrane stabilizing activity.

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