Inhibition of β-ARK1 Ameliorates Morphine-induced Tolerance and Hyperalgesia Via Modulating the Activity of Spinal NMDA Receptors
Our previous study has proposed that increased presynaptic NMDARs activities play pivotal roles in the development of opioid tolerance and hyperalgesia, and blocking spinal NMDARs attenuates chronic morphine-induced synaptic plasticity and behavior. However, the cellular signaling mechanisms remain...
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| Veröffentlicht in: | Molecular neurobiology 2018-06, Vol.55 (6), p.5393-5407 |
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| creator | Zhang, Xue Chen, Shaorui Chen, Hong Pan, Huilin Zhao, Yilin |
| description | Our previous study has proposed that increased presynaptic NMDARs activities play pivotal roles in the development of opioid tolerance and hyperalgesia, and blocking spinal NMDARs attenuates chronic morphine-induced synaptic plasticity and behavior. However, the cellular signaling mechanisms remain to be investigated. The aim of this research was to address the role of β-ARK1 in opioid analgesia. Opioid tolerance and hyperalgesia was induced by daily systemic morphine injections in rats for eight consecutive days. Whole-cell voltage-clamp was employed to record spontaneous EPSCs and evoked-AMPA-EPSCs in dorsal lamina II neurons. Strikingly, brief application of 1 μM morphine decreased the percentage of inhibition and was followed by a large LTP in the amplitude of monosynaptic evoked-AMPA-EPSCs in opioid-tolerant rats. There was no effect on these responses by postsynaptic dialysis of the G-protein inhibitor. Incubation with the NMDAR blocker AP5 potentiated morphine-induced inhibition and attenuated washout potentiation after cessation of morphine in the amplitude of AMPA-EPSCs. Incubation with β-ARK1 inhibitor had the same effect on these responses. Incubation with β-ARK1 inhibitor diminished NMDAR hyperfunction-increased glutamatergic synaptic transmission and enhanced the analgesic effect of morphine. Intrathecal injections of β-ARK1 inhibitor significantly attenuated opioid-induced hyperalgesia and tolerance. β-ARK1 plays a pivotal role in the development and maintenance of opioid tolerance and hyperalgesia. Blockade of β-ARK1 activation ameliorates morphine tolerance and hyperalgesia via regulating the activity of spinal NMDARs. These findings provide electrophysiological evidence and useful insights regarding the mechanistic action of β-ARK1 inhibitor as a potential anti-hyperalgesic agent to improve the efficacy of opioid therapies. |
| doi_str_mv | 10.1007/s12035-017-0780-3 |
| format | Article |
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However, the cellular signaling mechanisms remain to be investigated. The aim of this research was to address the role of β-ARK1 in opioid analgesia. Opioid tolerance and hyperalgesia was induced by daily systemic morphine injections in rats for eight consecutive days. Whole-cell voltage-clamp was employed to record spontaneous EPSCs and evoked-AMPA-EPSCs in dorsal lamina II neurons. Strikingly, brief application of 1 μM morphine decreased the percentage of inhibition and was followed by a large LTP in the amplitude of monosynaptic evoked-AMPA-EPSCs in opioid-tolerant rats. There was no effect on these responses by postsynaptic dialysis of the G-protein inhibitor. Incubation with the NMDAR blocker AP5 potentiated morphine-induced inhibition and attenuated washout potentiation after cessation of morphine in the amplitude of AMPA-EPSCs. Incubation with β-ARK1 inhibitor had the same effect on these responses. Incubation with β-ARK1 inhibitor diminished NMDAR hyperfunction-increased glutamatergic synaptic transmission and enhanced the analgesic effect of morphine. Intrathecal injections of β-ARK1 inhibitor significantly attenuated opioid-induced hyperalgesia and tolerance. β-ARK1 plays a pivotal role in the development and maintenance of opioid tolerance and hyperalgesia. Blockade of β-ARK1 activation ameliorates morphine tolerance and hyperalgesia via regulating the activity of spinal NMDARs. These findings provide electrophysiological evidence and useful insights regarding the mechanistic action of β-ARK1 inhibitor as a potential anti-hyperalgesic agent to improve the efficacy of opioid therapies.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-017-0780-3</identifier><identifier>PMID: 28975565</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Analgesia ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Dialysis ; Drug tolerance ; Excitatory postsynaptic potentials ; G-Protein-Coupled Receptor Kinase 2 - antagonists & inhibitors ; G-Protein-Coupled Receptor Kinase 2 - metabolism ; Glutamatergic transmission ; Glutamates - metabolism ; Glutamic acid receptors (ionotropic) ; Hyperalgesia ; Hyperalgesia - metabolism ; Hyperalgesia - pathology ; Hyperalgesia - physiopathology ; Inhibition ; Long-term potentiation ; Male ; Morphine ; Morphine - pharmacology ; N-Methyl-D-aspartic acid receptors ; Narcotics ; Neurobiology ; Neurology ; Neurosciences ; Opioids ; Pain perception ; Presynaptic Terminals - drug effects ; Presynaptic Terminals - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate - metabolism ; Rodents ; Spinal Cord - pathology ; Spinal plasticity ; Synaptic plasticity ; Synaptic transmission ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</subject><ispartof>Molecular neurobiology, 2018-06, Vol.55 (6), p.5393-5407</ispartof><rights>Springer Science+Business Media, LLC 2017</rights><rights>Molecular Neurobiology is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-782d96eed33625a9d094753cbc340fb7663c5b6cf920f7b8dc6e598d057aee603</citedby><cites>FETCH-LOGICAL-c372t-782d96eed33625a9d094753cbc340fb7663c5b6cf920f7b8dc6e598d057aee603</cites><orcidid>0000-0003-2587-0400</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-017-0780-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-017-0780-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28975565$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Xue</creatorcontrib><creatorcontrib>Chen, Shaorui</creatorcontrib><creatorcontrib>Chen, Hong</creatorcontrib><creatorcontrib>Pan, Huilin</creatorcontrib><creatorcontrib>Zhao, Yilin</creatorcontrib><title>Inhibition of β-ARK1 Ameliorates Morphine-induced Tolerance and Hyperalgesia Via Modulating the Activity of Spinal NMDA Receptors</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Our previous study has proposed that increased presynaptic NMDARs activities play pivotal roles in the development of opioid tolerance and hyperalgesia, and blocking spinal NMDARs attenuates chronic morphine-induced synaptic plasticity and behavior. However, the cellular signaling mechanisms remain to be investigated. The aim of this research was to address the role of β-ARK1 in opioid analgesia. Opioid tolerance and hyperalgesia was induced by daily systemic morphine injections in rats for eight consecutive days. Whole-cell voltage-clamp was employed to record spontaneous EPSCs and evoked-AMPA-EPSCs in dorsal lamina II neurons. Strikingly, brief application of 1 μM morphine decreased the percentage of inhibition and was followed by a large LTP in the amplitude of monosynaptic evoked-AMPA-EPSCs in opioid-tolerant rats. There was no effect on these responses by postsynaptic dialysis of the G-protein inhibitor. Incubation with the NMDAR blocker AP5 potentiated morphine-induced inhibition and attenuated washout potentiation after cessation of morphine in the amplitude of AMPA-EPSCs. Incubation with β-ARK1 inhibitor had the same effect on these responses. Incubation with β-ARK1 inhibitor diminished NMDAR hyperfunction-increased glutamatergic synaptic transmission and enhanced the analgesic effect of morphine. Intrathecal injections of β-ARK1 inhibitor significantly attenuated opioid-induced hyperalgesia and tolerance. β-ARK1 plays a pivotal role in the development and maintenance of opioid tolerance and hyperalgesia. Blockade of β-ARK1 activation ameliorates morphine tolerance and hyperalgesia via regulating the activity of spinal NMDARs. These findings provide electrophysiological evidence and useful insights regarding the mechanistic action of β-ARK1 inhibitor as a potential anti-hyperalgesic agent to improve the efficacy of opioid therapies.</description><subject>Analgesia</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Dialysis</subject><subject>Drug tolerance</subject><subject>Excitatory postsynaptic potentials</subject><subject>G-Protein-Coupled Receptor Kinase 2 - antagonists & inhibitors</subject><subject>G-Protein-Coupled Receptor Kinase 2 - metabolism</subject><subject>Glutamatergic transmission</subject><subject>Glutamates - metabolism</subject><subject>Glutamic acid receptors (ionotropic)</subject><subject>Hyperalgesia</subject><subject>Hyperalgesia - metabolism</subject><subject>Hyperalgesia - pathology</subject><subject>Hyperalgesia - physiopathology</subject><subject>Inhibition</subject><subject>Long-term potentiation</subject><subject>Male</subject><subject>Morphine</subject><subject>Morphine - pharmacology</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Narcotics</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Opioids</subject><subject>Pain perception</subject><subject>Presynaptic Terminals - drug effects</subject><subject>Presynaptic Terminals - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Rodents</subject><subject>Spinal Cord - pathology</subject><subject>Spinal plasticity</subject><subject>Synaptic plasticity</subject><subject>Synaptic transmission</subject><subject>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc-KFDEQh4Mo7rj6AF4k4MVLNH8mnc5xWHV3cUdhXb2GdFI9k6UnaZNuYa77SD6Iz2SGWRUED6EI-epXoT6EnjP6mlGq3hTGqZCEMkWoaikRD9CCSakJYy1_iBa01YKoZtmeoCel3FLKOaPqMTrhrVZSNnKB7i7jNnRhCini1OOfP8jq-gPDqx0MIWU7QcHrlMdtiEBC9LMDj2_SANlGB9hGjy_2Y70NGyjB4q_1rJOfBzuFuMHTFvDKTeF7mPaH-M9jiHbAH9dvV_gaHIxTyuUpetTbocCz-3qKvrx_d3N2Qa4-nV-era6IE4pPRLXc6wbAC9FwabWneqmkcJ0TS9p3qmmEk13jes1pr7rWuwakbj2VygI0VJyiV8fcMadvM5TJ7EJxMAw2QpqLYTWP6lZpWdGX_6C3ac7168XUjSsh6ZLxSrEj5XIqJUNvxhx2Nu8No-YgyBwFmSrIHAQZUXte3CfP3Q78n47fRirAj0CpT3ED-e_o_6f-AtSPm7Y</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Zhang, Xue</creator><creator>Chen, Shaorui</creator><creator>Chen, Hong</creator><creator>Pan, Huilin</creator><creator>Zhao, Yilin</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2587-0400</orcidid></search><sort><creationdate>20180601</creationdate><title>Inhibition of β-ARK1 Ameliorates Morphine-induced Tolerance and Hyperalgesia Via Modulating the Activity of Spinal NMDA Receptors</title><author>Zhang, Xue ; Chen, Shaorui ; Chen, Hong ; Pan, Huilin ; Zhao, Yilin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-782d96eed33625a9d094753cbc340fb7663c5b6cf920f7b8dc6e598d057aee603</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Analgesia</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Dialysis</topic><topic>Drug tolerance</topic><topic>Excitatory postsynaptic potentials</topic><topic>G-Protein-Coupled Receptor Kinase 2 - antagonists & inhibitors</topic><topic>G-Protein-Coupled Receptor Kinase 2 - metabolism</topic><topic>Glutamatergic transmission</topic><topic>Glutamates - metabolism</topic><topic>Glutamic acid receptors (ionotropic)</topic><topic>Hyperalgesia</topic><topic>Hyperalgesia - metabolism</topic><topic>Hyperalgesia - pathology</topic><topic>Hyperalgesia - physiopathology</topic><topic>Inhibition</topic><topic>Long-term potentiation</topic><topic>Male</topic><topic>Morphine</topic><topic>Morphine - pharmacology</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Narcotics</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Opioids</topic><topic>Pain perception</topic><topic>Presynaptic Terminals - drug effects</topic><topic>Presynaptic Terminals - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Rodents</topic><topic>Spinal Cord - pathology</topic><topic>Spinal plasticity</topic><topic>Synaptic plasticity</topic><topic>Synaptic transmission</topic><topic>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xue</creatorcontrib><creatorcontrib>Chen, Shaorui</creatorcontrib><creatorcontrib>Chen, Hong</creatorcontrib><creatorcontrib>Pan, Huilin</creatorcontrib><creatorcontrib>Zhao, Yilin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Xue</au><au>Chen, Shaorui</au><au>Chen, Hong</au><au>Pan, Huilin</au><au>Zhao, Yilin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of β-ARK1 Ameliorates Morphine-induced Tolerance and Hyperalgesia Via Modulating the Activity of Spinal NMDA Receptors</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>55</volume><issue>6</issue><spage>5393</spage><epage>5407</epage><pages>5393-5407</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Our previous study has proposed that increased presynaptic NMDARs activities play pivotal roles in the development of opioid tolerance and hyperalgesia, and blocking spinal NMDARs attenuates chronic morphine-induced synaptic plasticity and behavior. However, the cellular signaling mechanisms remain to be investigated. The aim of this research was to address the role of β-ARK1 in opioid analgesia. Opioid tolerance and hyperalgesia was induced by daily systemic morphine injections in rats for eight consecutive days. Whole-cell voltage-clamp was employed to record spontaneous EPSCs and evoked-AMPA-EPSCs in dorsal lamina II neurons. Strikingly, brief application of 1 μM morphine decreased the percentage of inhibition and was followed by a large LTP in the amplitude of monosynaptic evoked-AMPA-EPSCs in opioid-tolerant rats. There was no effect on these responses by postsynaptic dialysis of the G-protein inhibitor. Incubation with the NMDAR blocker AP5 potentiated morphine-induced inhibition and attenuated washout potentiation after cessation of morphine in the amplitude of AMPA-EPSCs. Incubation with β-ARK1 inhibitor had the same effect on these responses. Incubation with β-ARK1 inhibitor diminished NMDAR hyperfunction-increased glutamatergic synaptic transmission and enhanced the analgesic effect of morphine. Intrathecal injections of β-ARK1 inhibitor significantly attenuated opioid-induced hyperalgesia and tolerance. β-ARK1 plays a pivotal role in the development and maintenance of opioid tolerance and hyperalgesia. Blockade of β-ARK1 activation ameliorates morphine tolerance and hyperalgesia via regulating the activity of spinal NMDARs. These findings provide electrophysiological evidence and useful insights regarding the mechanistic action of β-ARK1 inhibitor as a potential anti-hyperalgesic agent to improve the efficacy of opioid therapies.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28975565</pmid><doi>10.1007/s12035-017-0780-3</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-2587-0400</orcidid></addata></record> |
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| subjects | Analgesia Animals Biomedical and Life Sciences Biomedicine Cell Biology Dialysis Drug tolerance Excitatory postsynaptic potentials G-Protein-Coupled Receptor Kinase 2 - antagonists & inhibitors G-Protein-Coupled Receptor Kinase 2 - metabolism Glutamatergic transmission Glutamates - metabolism Glutamic acid receptors (ionotropic) Hyperalgesia Hyperalgesia - metabolism Hyperalgesia - pathology Hyperalgesia - physiopathology Inhibition Long-term potentiation Male Morphine Morphine - pharmacology N-Methyl-D-aspartic acid receptors Narcotics Neurobiology Neurology Neurosciences Opioids Pain perception Presynaptic Terminals - drug effects Presynaptic Terminals - metabolism Rats Rats, Sprague-Dawley Receptors, N-Methyl-D-Aspartate - metabolism Rodents Spinal Cord - pathology Spinal plasticity Synaptic plasticity Synaptic transmission α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid |
| title | Inhibition of β-ARK1 Ameliorates Morphine-induced Tolerance and Hyperalgesia Via Modulating the Activity of Spinal NMDA Receptors |
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