Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction
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| internalnotes | Abdel-Zaher AO, Abdel-Rahman MS, and Elwasei FM. Blockade of Nitric Oxide Overproduction and Oxidative Stress by Nigella sativa Oil Attenuates Morphine-Induced Tolerance and Dependence in Mice. Neurochem Res. 2010; 35:1557–1565. Antkiewicz-Michaluk L. Voltage-operated calcium channels: characteristics and their role in the mechanism of action of psychotropic drugs. Pol. J. Pharmacol. 1999; 51: 179-86. Bajo M, Crawford EF, Roberto M, Madamba SG, and Siggins GR. Chronic morphine treatment alters expression of N-methyl-D-aspartate receptor sub-units in the extended amygdale. J Neurosci. Res. 2006; 83: 532–537. Belcheva MM, Clerk AL, Haas PD, Serna JS, Hahn JW, Kiss A and Coscia CJ. µ and к Opioid Receptors Activate ERK/MAPK via Different Protein Kinase C Isoforms and Secondary Messengers in Astrocytes. The Journal of biological chemistry. 2005; 280(30): 27662-9. Berridge MJ. Elementary and Global aspects of calcium signalling. The Journal of Experimental Biol. 1997; 200: 315–319. Bhat RS, Bhaskaran M, Mongia A, Hitosugi N, and Singhal PC. Morphine-induced macrophage apoptosis: oxidative stress and strategies for modulation. J. Leukoc. Biol. 2004; 75 (6): 1131-1138. Bilecki W, Zapart G, Ligęza A, Wawrzczak-Bargiela A, Urbański MJ and Przewłocki R. Regulation of the extracellular signal-regulated kinases following acute and chronic opioid treatment. Cell. Mol. Life Sci. 2005; 62: 2369–2375. Bogeski I, Kappl R, Kummerow C, Gulaboski R, Hoth M, Niemeyer BA: Redox regulation of calcium ion channels: chemical and physiological aspects. Cell Calcium. 2011; 50(5):407–423. Bortolotto ZA and Collingridge GL. Involvement of calcium/ calmodulindependent protein kinases in the setting of a molecular switch involved in hippocampal LTP. Neuropharmacology. 1998; 37:535–544. Ermak G, Davies KJ: Calcium and oxidative stress: from cell signaling to cell death. Molecular Immunology. 2002, 38(10):713–721. Erondu NE and Kennedy MB. Regional distribution of type II Ca2+/calmodulin-dependent protein kinase in rat brain. J Neurosci. 1985; 5:3270–3277. Fan GH, Wang LZ, Qiu HC, Ma L, and Pei G. Inhibition of calcium/calmodulindependent protein kinase II in rat hippocampus attenuates morphine tolerance and dependence. Mol Pharmacol. 1999; 56:39–45. Fields A and Sarne Y. The stimulatory effect of opioids on cyclic AMP production in SK-N-SH cells is mediated by calcium ions. Life Sci. 1997; 61:595–602. Ghosh A, Greenberg ME. Calcium signaling in neurons: molecular mechanisms and cellular consequences. Science. 1998; 268: 239 -247. Gray AM, Rawls SM, Shippenberg TS, and McGinty JF. The k-Opioid Agonist, U-69593, Decreases Acute Amphetamine-Evoked Behaviors and Calcium-Dependent Dialysate Levels of Dopamine and Glutamate in the Ventral Striatum. J. Neurochem. 1999; 73: 1066–1074. Guzman D, Va´zquez I, Brizuela N, Alvarez R, Mejı´a G, Garcı´a E, Santamarı´a D, de Apreza M, and Olguı´n H. Assessment of oxidative damage induced by acute doses of morphine sulfate in postnatal and adult rat brain. Neurochem Res. 2006; 31: 549–554. Hanson PI and Schulman H. Neuronal Ca2+/calmodulin-dependent protein kinases. Ann Rev Biochem. 1992; 61: 559-601. Ivannikov MV and Macleod GT. "Mitochondrial Free Ca2+ Levels and Their Effects on Energy Metabolism in Drosophila Motor Nerve Terminals". J Biophys. 2013; 104 (11): 2353–2361. Liang D, Li X, and Clark JD. Increased expression of Ca2+/calmodulindependent protein kinase II alpha during chronic morphine exposure. Neuroscience. 2004; 123:769–775. Little HJ. The role of calcium channels in drug dependence. Drug Alcohol Depend. 1995; 38: 173-94. Lou LG, Zhou TH, Wang P and Pei G. Modulation of Ca2+/calmodulindependent protein kinase II activity by acute and chronic morphine administration in rat hippocampus: Differential regulation of a and b isoforms. Mol Pharmacol. 1999; 55:557–563. McDonald J. And Lambert D. Opioid receptors. Continuing Education in Anaesthesia, Critical care and Pain 2005; 5(1): 22-25. McCarberg BH and Barkin RL. Long-acting opioids for chronic pain: pharmacotherapeutic opportunities to enhance complaince, quality of life, and analgesia; Am. J. Therapeutics. 2001; 8: 181–186. Murray F, Harrison NJ, Grimwood S, Bristow LJ, Hutson PH. Nucleous accumben NMDA receptor subunit expression and function is enhanced in morphine-dependent rats. Eur J Pharmacol. 2007; 21: 191– 197. Nehmad R, Nadler H, and Simantov R. Effects of acute and chronic morphine treatment of calmodulin activity of rat brain. Mol Pharmacol. 1982; 22:389–394. Nestler EJ. Under Siege: The Brain on Opiates. Neuron. 1996; 16: 897–900. Nestler EJ. From neurobiology to treatment: Progress against addiction, nature neurosci. Supplement. 2002; 5: 1076-79. Nestler EJ. Molecular basis of long term plasticity underlying addiction. Nature reviews/neuroscience. 2001; 2: 119-128. North R A. Opioid actions on membrane ion channels. Hand book of Exp. Pharmacol. 1993; 104: 773–797. Pierce RC, Quick EA, Reeder DC, Morgan ZR and Kalivas PW. Calcium-Mediated Second Messengers Modulate the Expression of Behavioral Sensitization to Cocaine. The journal of pharmacology and experimental therapeutics. 1998; 286: 1171–1176. Piros ET, Hales TG, and Evans CJ. Functional analysis of cloned opioid receptors in transfected cell lines. Neurochem. Res. 1996; 21 (11): 1277-1285. Przewlocki R, Parsons KL, Sweeney D, Trotter C, Netzeband JG, Siggins GR, and Gruol DL. Opioid Enhancement of Calcium Oscillations and Burst Events Involving NMDA Receptors and L-Type Calcium Channels in Cultured Hippocampal Neurons. The Journal of Neurosci. 1999; 19(22): 9705–9715. Pu L, Bao G, Xu N, Ma L and Pei G. Hippocampal Long-Term Potentiation Is Reduced by Chronic Opiate Treatment and Can Be Restored by Re-Exposure to Opiates. The Journal of Neuroscience. 2002; 22 (5): 1914–1921. Quillan JM, Carlson KW, Song C, Wang D, and Sadee W. Differential effects of mu-opioid receptor ligands on Ca2+ signaling. J Pharmacol Exp Ther. 2002; 302:1002–1012. Rabbani M, Jafarian A and Sobhanian MH. Comparison of acute and chronic effects of nifedipine on naloxone precipitated morphine withdrawal in mice. J. Islamic Rep. Iran. 2003; 17 (3): 251-257. Rabbani M, Jafarian A and Ahmadi A. Acute and Chronic effect of nitrendipine on naloxone precipitated morphine withdrawal in mice. Iranian Journal of Pharmaceutical Research. 2004; 2: 109-114. Saboory E, Ghazizadeh V, Heshmatian B and Khademansari MH. Desmopressin accelerates the rate of urinary morphine excretion and attenuates withdrawal symptoms in rats. Psychiatry and Clinical Neurosciences.2012; 66: 594–601. Samarghandian S, Afshari R and Farkhonden T. Effect of longterm treatment of morphine on enzymes oxidative stress indices and antioxidant status in male rats liver. Int J Clin Exp Med. 2013; 7(4): 1449-53. Schulman H. The multifunctional Ca2+/calmodulin-dependent protein kinases. Curr Opin Cell Biol. 1993; 5:247–253. Seth V, Upadyaya P, Moghe V and Ahmad M. Role of calcium in morphine dependence and naloxone-precipitated withdrawal in mice. Journal of Experimental Pharmacology. 2011; 3: 7–12. Siesjo BK. Calcium-mediated processes in neuronal degeneration. Ann NY Acad Sci. 1994; 747:140 –161. Skrabalova J, Drastichova Z and Novotny J. Morphine as a Potential Oxidative Stress-Causing Agent. Mini-Reviews in Organic Chemistry. 2013; 10: 367-372. Smith M T, Cabot P J, Ross F B, Robertson A D and Lewis R J. The novel N-type calcium channel blocker, AM336, produces potent dose-dependent antinociception after intrathecal dosing in rats and inhibits substance P release in rat spinal cord slices; Pain. 2002; 96: 119–127. Sumathi T, Nathiya VC, and Sakthikumar M. Protective effect of bacoside-A against morphine-induced oxidative stress in rats. Indian J Pharm Sci. 2011; 73: 409-15. Tang L, Shukla PK, Wang LX and Wang ZJ. Reversal of Morphine Antinociceptive Tolerance and Dependence by the Acute Supraspinal Inhibition of Ca2+/Calmodulin-Dependent Protein Kinase II. J Pharmacol Exp Ther. 2006; 317 : 901-909. Tang T, Chang C, Wang H, Erickson JD, Reichard RA, Martin AG, Shannon EK, Martin AL, Huang Y and Aronstam RS. Oxidative stress disruption of receptor-mediated calcium signaling mechanisms. J Biomedical Science. 2013; 20:48. Tsien RW, Lipscombe D, Madison DV, Bley KR and Fox AP. Multiple types of neuronal calcium channels and their selective modulation. Trends Neurosci. 1988; 11: 431-8. Williams JT, Christie MJ and Manzoni O. Cellular and synaptic adaptations mediating opioid dependence. Physiol Rev. 2001; 81: 299- 343. Verma V, Mediratta PK and Sharma KK. Potentiation of analgesic and reversal of tolerance to morphine by calcium channel blockers. Indian Journal of Experimental Biology. 2001; 39: 636-642. Xu B, Wang Z, Li G, Li B, Lin H, Zheng R and Zheng Q. Heroin Administered Mice Involved in Oxidative Stress and Exogenous Antioxidant-Alleviated Withdrawal Syndrome. Basic & Clinical Pharmacology & Toxicol. 2006;99: 153–161. Yamamoto H, Harris RA, Loh HH, Way EL. Effects of acute and chronic morphine treatments on calcium localization and binding in brain. J Pharmacol Exp Ther. 1978;205:255–264. Yoshikawa T and Naito Y. What Is Oxidative Stress. JMAJ. 2002; 45 (7): 271–276. Yung LM, Leung FP, Yao X, Chen ZY, and Huang Y. Reactive oxygen species in vascular wall. Cardiovasc. Hematol. Disord. Drug Targets. 2006; 6 (1): 1-19. Zhang Y, Zheng Q, Pan J and Zheng R. Oxidative Damage of Biomolecules in Mouse Liver Induced by Morphine and Protected by Antioxidants. Basic & Clinical Pharmacol. Toxicol. 2004; 95: 53–58. Zima AV, Blatter LA: Redox regulation of cardiac calcium channels and transporters. Cardiovascular Research 2006, 71(2):310–321. Zhou J, Li Y, Yan G, Bu Q, Lv L, Yang Y, Zhao J, Shao X, Deng Y, Zhu R, Zhao Y, and Cen X. Protective role of taurine against morphine-induced neurotoxicity in C6 cells via inhibition of oxidative stress. Neurotox. Res. 2011; 20: 334–342. Zhou JF, Yan XF, Ruan ZR, Peng FY, Cai D, Yuan H, et al. Heroin abuse and nitric oxide, oxidation, peroxidation, lipid peroxidation. Biomed Environ Sci 2000;13: 131-9. |
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| spelling | 11568 https://intelek.unisza.edu.my/intelek/pages/view.php?ref=11568 https://intelek.unisza.edu.my/intelek/pages/search.php?search=!collection407072 Restricted Document Article Journal UniSZA Unisza unisza image/jpeg inches 96 96 756 87 87 2015-03-08 11:39:41 1435x756 1435 5824-01-FH02-FPSK-15-02624.jpg UniSZA Private Access Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction Journal of Applied Pharmaceutical Science Addiction and withdrawal are problems disturbing the health of the individual and also causes difficulties for society, raising the rates of divorce, unemployment and government spending on legal and medical systems. Opioids show an important pharmacological effect in the treatment of pain, with extremely addictive potential. Chronic opioid exposure is known to produce the complex behaviors of tolerance and dependence, a state exposed by opioid abstinence leading to withdrawal syndrome, as well as oxidative stress. Studies show that calcium mediated secondary messengers play a crucial role in the mechanism of addictive process and oxidative stress induced by chronic opioid usage. Calcium/calmodulin-dependent protein kinase II (CaMKII), is a major calcium regulated signal transducer that controls many neuronal systems and play important role in neuronal plasticity and can act as a key and direct promoting opioid tolerance and dependence and identifying such a direct mechanism may be useful for designing a pharmacology treatment for these conditions, recent studies, has been shown that calcium channels antagonist can be used in the treatment of withdrawal syndrome. Chronic opioid exposure associated with tolerance, dependence withdrawal syndrome and oxidative stress. Studies has shown that calcium mediated secondary messengers involved in the genesis of these conditions, better understanding of biological mechanisms underlie reduction in neuronal cell excitability could help in the identification of pharmacological targets for treatment. 5 1 114-119 Abdel-Zaher AO, Abdel-Rahman MS, and Elwasei FM. Blockade of Nitric Oxide Overproduction and Oxidative Stress by Nigella sativa Oil Attenuates Morphine-Induced Tolerance and Dependence in Mice. Neurochem Res. 2010; 35:1557–1565. Antkiewicz-Michaluk L. Voltage-operated calcium channels: characteristics and their role in the mechanism of action of psychotropic drugs. Pol. J. Pharmacol. 1999; 51: 179-86. Bajo M, Crawford EF, Roberto M, Madamba SG, and Siggins GR. Chronic morphine treatment alters expression of N-methyl-D-aspartate receptor sub-units in the extended amygdale. J Neurosci. Res. 2006; 83: 532–537. Belcheva MM, Clerk AL, Haas PD, Serna JS, Hahn JW, Kiss A and Coscia CJ. µ and к Opioid Receptors Activate ERK/MAPK via Different Protein Kinase C Isoforms and Secondary Messengers in Astrocytes. The Journal of biological chemistry. 2005; 280(30): 27662-9. Berridge MJ. Elementary and Global aspects of calcium signalling. The Journal of Experimental Biol. 1997; 200: 315–319. Bhat RS, Bhaskaran M, Mongia A, Hitosugi N, and Singhal PC. Morphine-induced macrophage apoptosis: oxidative stress and strategies for modulation. J. Leukoc. Biol. 2004; 75 (6): 1131-1138. Bilecki W, Zapart G, Ligęza A, Wawrzczak-Bargiela A, Urbański MJ and Przewłocki R. Regulation of the extracellular signal-regulated kinases following acute and chronic opioid treatment. Cell. Mol. Life Sci. 2005; 62: 2369–2375. Bogeski I, Kappl R, Kummerow C, Gulaboski R, Hoth M, Niemeyer BA: Redox regulation of calcium ion channels: chemical and physiological aspects. Cell Calcium. 2011; 50(5):407–423. Bortolotto ZA and Collingridge GL. Involvement of calcium/ calmodulindependent protein kinases in the setting of a molecular switch involved in hippocampal LTP. Neuropharmacology. 1998; 37:535–544. Ermak G, Davies KJ: Calcium and oxidative stress: from cell signaling to cell death. Molecular Immunology. 2002, 38(10):713–721. Erondu NE and Kennedy MB. Regional distribution of type II Ca2+/calmodulin-dependent protein kinase in rat brain. J Neurosci. 1985; 5:3270–3277. Fan GH, Wang LZ, Qiu HC, Ma L, and Pei G. Inhibition of calcium/calmodulindependent protein kinase II in rat hippocampus attenuates morphine tolerance and dependence. Mol Pharmacol. 1999; 56:39–45. Fields A and Sarne Y. The stimulatory effect of opioids on cyclic AMP production in SK-N-SH cells is mediated by calcium ions. Life Sci. 1997; 61:595–602. Ghosh A, Greenberg ME. Calcium signaling in neurons: molecular mechanisms and cellular consequences. Science. 1998; 268: 239 -247. Gray AM, Rawls SM, Shippenberg TS, and McGinty JF. The k-Opioid Agonist, U-69593, Decreases Acute Amphetamine-Evoked Behaviors and Calcium-Dependent Dialysate Levels of Dopamine and Glutamate in the Ventral Striatum. J. Neurochem. 1999; 73: 1066–1074. Guzman D, Va´zquez I, Brizuela N, Alvarez R, Mejı´a G, Garcı´a E, Santamarı´a D, de Apreza M, and Olguı´n H. Assessment of oxidative damage induced by acute doses of morphine sulfate in postnatal and adult rat brain. Neurochem Res. 2006; 31: 549–554. Hanson PI and Schulman H. Neuronal Ca2+/calmodulin-dependent protein kinases. Ann Rev Biochem. 1992; 61: 559-601. Ivannikov MV and Macleod GT. "Mitochondrial Free Ca2+ Levels and Their Effects on Energy Metabolism in Drosophila Motor Nerve Terminals". J Biophys. 2013; 104 (11): 2353–2361. Liang D, Li X, and Clark JD. Increased expression of Ca2+/calmodulindependent protein kinase II alpha during chronic morphine exposure. Neuroscience. 2004; 123:769–775. Little HJ. The role of calcium channels in drug dependence. Drug Alcohol Depend. 1995; 38: 173-94. Lou LG, Zhou TH, Wang P and Pei G. Modulation of Ca2+/calmodulindependent protein kinase II activity by acute and chronic morphine administration in rat hippocampus: Differential regulation of a and b isoforms. Mol Pharmacol. 1999; 55:557–563. McDonald J. And Lambert D. Opioid receptors. Continuing Education in Anaesthesia, Critical care and Pain 2005; 5(1): 22-25. McCarberg BH and Barkin RL. Long-acting opioids for chronic pain: pharmacotherapeutic opportunities to enhance complaince, quality of life, and analgesia; Am. J. Therapeutics. 2001; 8: 181–186. Murray F, Harrison NJ, Grimwood S, Bristow LJ, Hutson PH. Nucleous accumben NMDA receptor subunit expression and function is enhanced in morphine-dependent rats. Eur J Pharmacol. 2007; 21: 191– 197. Nehmad R, Nadler H, and Simantov R. Effects of acute and chronic morphine treatment of calmodulin activity of rat brain. Mol Pharmacol. 1982; 22:389–394. Nestler EJ. Under Siege: The Brain on Opiates. Neuron. 1996; 16: 897–900. Nestler EJ. From neurobiology to treatment: Progress against addiction, nature neurosci. Supplement. 2002; 5: 1076-79. Nestler EJ. Molecular basis of long term plasticity underlying addiction. Nature reviews/neuroscience. 2001; 2: 119-128. North R A. Opioid actions on membrane ion channels. Hand book of Exp. Pharmacol. 1993; 104: 773–797. Pierce RC, Quick EA, Reeder DC, Morgan ZR and Kalivas PW. Calcium-Mediated Second Messengers Modulate the Expression of Behavioral Sensitization to Cocaine. The journal of pharmacology and experimental therapeutics. 1998; 286: 1171–1176. Piros ET, Hales TG, and Evans CJ. Functional analysis of cloned opioid receptors in transfected cell lines. Neurochem. Res. 1996; 21 (11): 1277-1285. Przewlocki R, Parsons KL, Sweeney D, Trotter C, Netzeband JG, Siggins GR, and Gruol DL. Opioid Enhancement of Calcium Oscillations and Burst Events Involving NMDA Receptors and L-Type Calcium Channels in Cultured Hippocampal Neurons. The Journal of Neurosci. 1999; 19(22): 9705–9715. Pu L, Bao G, Xu N, Ma L and Pei G. Hippocampal Long-Term Potentiation Is Reduced by Chronic Opiate Treatment and Can Be Restored by Re-Exposure to Opiates. The Journal of Neuroscience. 2002; 22 (5): 1914–1921. Quillan JM, Carlson KW, Song C, Wang D, and Sadee W. Differential effects of mu-opioid receptor ligands on Ca2+ signaling. J Pharmacol Exp Ther. 2002; 302:1002–1012. Rabbani M, Jafarian A and Sobhanian MH. Comparison of acute and chronic effects of nifedipine on naloxone precipitated morphine withdrawal in mice. J. Islamic Rep. Iran. 2003; 17 (3): 251-257. Rabbani M, Jafarian A and Ahmadi A. Acute and Chronic effect of nitrendipine on naloxone precipitated morphine withdrawal in mice. Iranian Journal of Pharmaceutical Research. 2004; 2: 109-114. Saboory E, Ghazizadeh V, Heshmatian B and Khademansari MH. Desmopressin accelerates the rate of urinary morphine excretion and attenuates withdrawal symptoms in rats. Psychiatry and Clinical Neurosciences.2012; 66: 594–601. Samarghandian S, Afshari R and Farkhonden T. Effect of longterm treatment of morphine on enzymes oxidative stress indices and antioxidant status in male rats liver. Int J Clin Exp Med. 2013; 7(4): 1449-53. Schulman H. The multifunctional Ca2+/calmodulin-dependent protein kinases. Curr Opin Cell Biol. 1993; 5:247–253. Seth V, Upadyaya P, Moghe V and Ahmad M. Role of calcium in morphine dependence and naloxone-precipitated withdrawal in mice. Journal of Experimental Pharmacology. 2011; 3: 7–12. Siesjo BK. Calcium-mediated processes in neuronal degeneration. Ann NY Acad Sci. 1994; 747:140 –161. Skrabalova J, Drastichova Z and Novotny J. Morphine as a Potential Oxidative Stress-Causing Agent. Mini-Reviews in Organic Chemistry. 2013; 10: 367-372. Smith M T, Cabot P J, Ross F B, Robertson A D and Lewis R J. The novel N-type calcium channel blocker, AM336, produces potent dose-dependent antinociception after intrathecal dosing in rats and inhibits substance P release in rat spinal cord slices; Pain. 2002; 96: 119–127. Sumathi T, Nathiya VC, and Sakthikumar M. Protective effect of bacoside-A against morphine-induced oxidative stress in rats. Indian J Pharm Sci. 2011; 73: 409-15. Tang L, Shukla PK, Wang LX and Wang ZJ. Reversal of Morphine Antinociceptive Tolerance and Dependence by the Acute Supraspinal Inhibition of Ca2+/Calmodulin-Dependent Protein Kinase II. J Pharmacol Exp Ther. 2006; 317 : 901-909. Tang T, Chang C, Wang H, Erickson JD, Reichard RA, Martin AG, Shannon EK, Martin AL, Huang Y and Aronstam RS. Oxidative stress disruption of receptor-mediated calcium signaling mechanisms. J Biomedical Science. 2013; 20:48. Tsien RW, Lipscombe D, Madison DV, Bley KR and Fox AP. Multiple types of neuronal calcium channels and their selective modulation. Trends Neurosci. 1988; 11: 431-8. Williams JT, Christie MJ and Manzoni O. Cellular and synaptic adaptations mediating opioid dependence. Physiol Rev. 2001; 81: 299- 343. Verma V, Mediratta PK and Sharma KK. Potentiation of analgesic and reversal of tolerance to morphine by calcium channel blockers. Indian Journal of Experimental Biology. 2001; 39: 636-642. Xu B, Wang Z, Li G, Li B, Lin H, Zheng R and Zheng Q. Heroin Administered Mice Involved in Oxidative Stress and Exogenous Antioxidant-Alleviated Withdrawal Syndrome. Basic & Clinical Pharmacology & Toxicol. 2006;99: 153–161. Yamamoto H, Harris RA, Loh HH, Way EL. Effects of acute and chronic morphine treatments on calcium localization and binding in brain. J Pharmacol Exp Ther. 1978;205:255–264. Yoshikawa T and Naito Y. What Is Oxidative Stress. JMAJ. 2002; 45 (7): 271–276. Yung LM, Leung FP, Yao X, Chen ZY, and Huang Y. Reactive oxygen species in vascular wall. Cardiovasc. Hematol. Disord. Drug Targets. 2006; 6 (1): 1-19. Zhang Y, Zheng Q, Pan J and Zheng R. Oxidative Damage of Biomolecules in Mouse Liver Induced by Morphine and Protected by Antioxidants. Basic & Clinical Pharmacol. Toxicol. 2004; 95: 53–58. Zima AV, Blatter LA: Redox regulation of cardiac calcium channels and transporters. Cardiovascular Research 2006, 71(2):310–321. Zhou J, Li Y, Yan G, Bu Q, Lv L, Yang Y, Zhao J, Shao X, Deng Y, Zhu R, Zhao Y, and Cen X. Protective role of taurine against morphine-induced neurotoxicity in C6 cells via inhibition of oxidative stress. Neurotox. Res. 2011; 20: 334–342. Zhou JF, Yan XF, Ruan ZR, Peng FY, Cai D, Yuan H, et al. Heroin abuse and nitric oxide, oxidation, peroxidation, lipid peroxidation. Biomed Environ Sci 2000;13: 131-9. |
| spellingShingle | Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction |
| summary | Addiction and withdrawal are problems disturbing the health of the individual and also causes difficulties for society, raising the rates of divorce, unemployment and government spending on legal and medical systems. Opioids show an important pharmacological effect in the treatment of pain, with extremely addictive potential. Chronic opioid exposure is known to produce the complex behaviors of tolerance and dependence, a state exposed by opioid abstinence leading to withdrawal syndrome, as well as oxidative stress. Studies show that calcium mediated secondary messengers play a crucial role in the mechanism of addictive process and oxidative stress induced by chronic opioid usage. Calcium/calmodulin-dependent protein kinase II (CaMKII), is a major calcium regulated signal transducer that controls many neuronal systems and play important role in neuronal plasticity and can act as a key and direct promoting opioid tolerance and dependence and identifying such a direct mechanism may be useful for designing a pharmacology treatment for these conditions, recent studies, has been shown that calcium channels antagonist can be used in the treatment of withdrawal syndrome. Chronic opioid exposure associated with tolerance, dependence withdrawal syndrome and oxidative stress. Studies has shown that calcium mediated secondary messengers involved in the genesis of these conditions, better understanding of biological mechanisms underlie reduction in neuronal cell excitability could help in the identification of pharmacological targets for treatment. |
| title | Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction |
| title_full | Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction |
| title_fullStr | Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction |
| title_full_unstemmed | Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction |
| title_short | Reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction |
| title_sort | reviews on calcium mediated secondary messengers in chronic opioids exposure/addiction |