Prosaptide D5 reverses hyperalgesia: inhibition of calcium channels through a pertussis toxin-sensitive G-protein mechanism in the rat
A retro-inverso 11-mer peptidomimetic of prosaposin, Prosaptide D5, induced neurite outgrowth in NS20Y neuroblastoma cells and enhanced [35S]GTPgammaS binding to rat synaptosomal membrane at low nanomolar concentrations similar to prosaposin. Intramuscular injection of D5 ameliorated thermal hyperal...
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| Veröffentlicht in: | Neuroscience letters 2000-01, Vol.278 (1-2), p.120-122 |
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| creator | Yan, L Otero, D A Hiraiwa, M O'Brien, J S |
| description | A retro-inverso 11-mer peptidomimetic of prosaposin, Prosaptide D5, induced neurite outgrowth in NS20Y neuroblastoma cells and enhanced [35S]GTPgammaS binding to rat synaptosomal membrane at low nanomolar concentrations similar to prosaposin. Intramuscular injection of D5 ameliorated thermal hyperalgesia in the Seltzer rat model of neuropathic pain, returning paw withdrawal latency to control levels within 3 h after treatment. The effect was sustained for at least 48 h after injection. Prosaposin and D5 inhibited K+-stimulated synaptosomal 45Ca2+ uptake similar to omega-conotoxin MVIIC, demonstrating that both effectors modulated voltage-dependent calcium channels (VDCC); inhibition was largely abolished by pretreatment with pertussis toxin before D5 treatment. The results suggest a mechanism whereby VDCC are modulated by a pertussis toxin-sensitive G-protein coupled receptor; D5 binds to this receptor and thereby ameliorates hyperalgesia in the Seltzer model of neuropathic pain. |
| doi_str_mv | 10.1016/s0304-3940(99)00902-7 |
| format | Article |
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Intramuscular injection of D5 ameliorated thermal hyperalgesia in the Seltzer rat model of neuropathic pain, returning paw withdrawal latency to control levels within 3 h after treatment. The effect was sustained for at least 48 h after injection. Prosaposin and D5 inhibited K+-stimulated synaptosomal 45Ca2+ uptake similar to omega-conotoxin MVIIC, demonstrating that both effectors modulated voltage-dependent calcium channels (VDCC); inhibition was largely abolished by pretreatment with pertussis toxin before D5 treatment. The results suggest a mechanism whereby VDCC are modulated by a pertussis toxin-sensitive G-protein coupled receptor; D5 binds to this receptor and thereby ameliorates hyperalgesia in the Seltzer model of neuropathic pain.</description><identifier>ISSN: 0304-3940</identifier><identifier>DOI: 10.1016/s0304-3940(99)00902-7</identifier><identifier>PMID: 10643816</identifier><language>eng</language><publisher>Ireland</publisher><subject>Animals ; Axotomy - adverse effects ; Calcium - metabolism ; Calcium Channels - drug effects ; Calcium Channels - metabolism ; GTP-Binding Proteins - drug effects ; GTP-Binding Proteins - physiology ; Guanosine 5'-O-(3-Thiotriphosphate) - metabolism ; Hyperalgesia - drug therapy ; Hyperalgesia - etiology ; Hyperalgesia - physiopathology ; Ion Channel Gating - drug effects ; Ion Transport - drug effects ; Male ; Nerve Growth Factors - pharmacology ; Nerve Growth Factors - therapeutic use ; Nerve Tissue Proteins - drug effects ; Nerve Tissue Proteins - physiology ; Neuralgia - complications ; Neuralgia - drug therapy ; Neuralgia - physiopathology ; Pertussis Toxin ; Rats ; Rats, Sprague-Dawley ; Reaction Time - drug effects ; Sciatic Nerve - injuries ; Synaptosomes - metabolism ; Virulence Factors, Bordetella - pharmacology</subject><ispartof>Neuroscience letters, 2000-01, Vol.278 (1-2), p.120-122</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c334t-cc1bd1ee0d3c8004e57b28bce64c0488eed6af9d5e9bc56359f53a2bd5e1d3873</citedby><cites>FETCH-LOGICAL-c334t-cc1bd1ee0d3c8004e57b28bce64c0488eed6af9d5e9bc56359f53a2bd5e1d3873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10643816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yan, L</creatorcontrib><creatorcontrib>Otero, D A</creatorcontrib><creatorcontrib>Hiraiwa, M</creatorcontrib><creatorcontrib>O'Brien, J S</creatorcontrib><title>Prosaptide D5 reverses hyperalgesia: inhibition of calcium channels through a pertussis toxin-sensitive G-protein mechanism in the rat</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>A retro-inverso 11-mer peptidomimetic of prosaposin, Prosaptide D5, induced neurite outgrowth in NS20Y neuroblastoma cells and enhanced [35S]GTPgammaS binding to rat synaptosomal membrane at low nanomolar concentrations similar to prosaposin. Intramuscular injection of D5 ameliorated thermal hyperalgesia in the Seltzer rat model of neuropathic pain, returning paw withdrawal latency to control levels within 3 h after treatment. The effect was sustained for at least 48 h after injection. Prosaposin and D5 inhibited K+-stimulated synaptosomal 45Ca2+ uptake similar to omega-conotoxin MVIIC, demonstrating that both effectors modulated voltage-dependent calcium channels (VDCC); inhibition was largely abolished by pretreatment with pertussis toxin before D5 treatment. The results suggest a mechanism whereby VDCC are modulated by a pertussis toxin-sensitive G-protein coupled receptor; D5 binds to this receptor and thereby ameliorates hyperalgesia in the Seltzer model of neuropathic pain.</description><subject>Animals</subject><subject>Axotomy - adverse effects</subject><subject>Calcium - metabolism</subject><subject>Calcium Channels - drug effects</subject><subject>Calcium Channels - metabolism</subject><subject>GTP-Binding Proteins - drug effects</subject><subject>GTP-Binding Proteins - physiology</subject><subject>Guanosine 5'-O-(3-Thiotriphosphate) - metabolism</subject><subject>Hyperalgesia - drug therapy</subject><subject>Hyperalgesia - etiology</subject><subject>Hyperalgesia - physiopathology</subject><subject>Ion Channel Gating - drug effects</subject><subject>Ion Transport - drug effects</subject><subject>Male</subject><subject>Nerve Growth Factors - pharmacology</subject><subject>Nerve Growth Factors - therapeutic use</subject><subject>Nerve Tissue Proteins - drug effects</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Neuralgia - complications</subject><subject>Neuralgia - drug therapy</subject><subject>Neuralgia - physiopathology</subject><subject>Pertussis Toxin</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reaction Time - drug effects</subject><subject>Sciatic Nerve - injuries</subject><subject>Synaptosomes - metabolism</subject><subject>Virulence Factors, Bordetella - pharmacology</subject><issn>0304-3940</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkE1P3DAQhn2gAgr8BJBPqD2kjNd2EvdWLS1UWgmkwtlynAkxysfWkyD2D_R312FR1dNIr-Z5Z_Qwdi7giwCRXxFIUJk0Cj4Z8xnAwCorDtjxv_iIfSR6BgAttDpkRwJyJUuRH7M_93Ekt51Cjfxa84gvGAmJt7stRtc9IQX3lYehDVWYwjjwseHedT7MPfetGwbsiE9tHOenljueoGkmCikbX8OQEQ6UuBfkN9k2jhOGgfe4gIH6VJtQ5NFNp-xD4zrCs_d5wh5_fH9Y32abu5uf62-bzEuppsx7UdUCEWrpSwCFuqhWZeUxVx5UWSLWuWtMrdFUXudSm0ZLt6pSIGpZFvKEXe570zO_Z6TJ9oE8dp0bcJzJFlAWpVEqLer9ok9-KGJjtzH0Lu6sALtIt78Wu3axa42xb9LtcuDi_cBc9Vj_R-2Ny79LFIM8</recordid><startdate>20000107</startdate><enddate>20000107</enddate><creator>Yan, L</creator><creator>Otero, D A</creator><creator>Hiraiwa, M</creator><creator>O'Brien, J S</creator><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>7X8</scope></search><sort><creationdate>20000107</creationdate><title>Prosaptide D5 reverses hyperalgesia: inhibition of calcium channels through a pertussis toxin-sensitive G-protein mechanism in the rat</title><author>Yan, L ; Otero, D A ; Hiraiwa, M ; O'Brien, J S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c334t-cc1bd1ee0d3c8004e57b28bce64c0488eed6af9d5e9bc56359f53a2bd5e1d3873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Axotomy - adverse effects</topic><topic>Calcium - metabolism</topic><topic>Calcium Channels - drug effects</topic><topic>Calcium Channels - metabolism</topic><topic>GTP-Binding Proteins - drug effects</topic><topic>GTP-Binding Proteins - physiology</topic><topic>Guanosine 5'-O-(3-Thiotriphosphate) - metabolism</topic><topic>Hyperalgesia - drug therapy</topic><topic>Hyperalgesia - etiology</topic><topic>Hyperalgesia - physiopathology</topic><topic>Ion Channel Gating - drug effects</topic><topic>Ion Transport - drug effects</topic><topic>Male</topic><topic>Nerve Growth Factors - pharmacology</topic><topic>Nerve Growth Factors - therapeutic use</topic><topic>Nerve Tissue Proteins - drug effects</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Neuralgia - complications</topic><topic>Neuralgia - drug therapy</topic><topic>Neuralgia - physiopathology</topic><topic>Pertussis Toxin</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reaction Time - drug effects</topic><topic>Sciatic Nerve - injuries</topic><topic>Synaptosomes - metabolism</topic><topic>Virulence Factors, Bordetella - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yan, L</creatorcontrib><creatorcontrib>Otero, D A</creatorcontrib><creatorcontrib>Hiraiwa, M</creatorcontrib><creatorcontrib>O'Brien, J S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yan, L</au><au>Otero, D A</au><au>Hiraiwa, M</au><au>O'Brien, J S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prosaptide D5 reverses hyperalgesia: inhibition of calcium channels through a pertussis toxin-sensitive G-protein mechanism in the rat</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2000-01-07</date><risdate>2000</risdate><volume>278</volume><issue>1-2</issue><spage>120</spage><epage>122</epage><pages>120-122</pages><issn>0304-3940</issn><abstract>A retro-inverso 11-mer peptidomimetic of prosaposin, Prosaptide D5, induced neurite outgrowth in NS20Y neuroblastoma cells and enhanced [35S]GTPgammaS binding to rat synaptosomal membrane at low nanomolar concentrations similar to prosaposin. Intramuscular injection of D5 ameliorated thermal hyperalgesia in the Seltzer rat model of neuropathic pain, returning paw withdrawal latency to control levels within 3 h after treatment. The effect was sustained for at least 48 h after injection. Prosaposin and D5 inhibited K+-stimulated synaptosomal 45Ca2+ uptake similar to omega-conotoxin MVIIC, demonstrating that both effectors modulated voltage-dependent calcium channels (VDCC); inhibition was largely abolished by pretreatment with pertussis toxin before D5 treatment. The results suggest a mechanism whereby VDCC are modulated by a pertussis toxin-sensitive G-protein coupled receptor; D5 binds to this receptor and thereby ameliorates hyperalgesia in the Seltzer model of neuropathic pain.</abstract><cop>Ireland</cop><pmid>10643816</pmid><doi>10.1016/s0304-3940(99)00902-7</doi><tpages>3</tpages></addata></record> |
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| source | Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE |
| subjects | Animals Axotomy - adverse effects Calcium - metabolism Calcium Channels - drug effects Calcium Channels - metabolism GTP-Binding Proteins - drug effects GTP-Binding Proteins - physiology Guanosine 5'-O-(3-Thiotriphosphate) - metabolism Hyperalgesia - drug therapy Hyperalgesia - etiology Hyperalgesia - physiopathology Ion Channel Gating - drug effects Ion Transport - drug effects Male Nerve Growth Factors - pharmacology Nerve Growth Factors - therapeutic use Nerve Tissue Proteins - drug effects Nerve Tissue Proteins - physiology Neuralgia - complications Neuralgia - drug therapy Neuralgia - physiopathology Pertussis Toxin Rats Rats, Sprague-Dawley Reaction Time - drug effects Sciatic Nerve - injuries Synaptosomes - metabolism Virulence Factors, Bordetella - pharmacology |
| title | Prosaptide D5 reverses hyperalgesia: inhibition of calcium channels through a pertussis toxin-sensitive G-protein mechanism in the rat |
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