The preventive and therapeutic effects of GCPII (NAALADase) inhibition on painful and sensory diabetic neuropathy
Excitotoxic glutamate release occurs in several neurological disorders. One source is derived from the hydrolysis of the neuropeptide N-acetyl aspartyl glutamate (NAAG) by glutamate carboxypeptidase II (GCPII, also known as NAALADase). Drugs that attenuate glutamate transmission have been shown to r...
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| Veröffentlicht in: | Journal of the neurological sciences 2006-09, Vol.247 (2), p.217-223 |
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| creator | Zhang, W. Murakawa, Y. Wozniak, K.M. Slusher, B. Sima, A.A.F. |
| description | Excitotoxic glutamate release occurs in several neurological disorders. One source is derived from the hydrolysis of the neuropeptide
N-acetyl aspartyl glutamate (NAAG) by glutamate carboxypeptidase II (GCPII, also known as NAALADase). Drugs that attenuate glutamate transmission have been shown to relieve neuropathic pain, however side effects have limited their clinical use. It appears that GCPII is exclusively recruited to provide a glutamate source in hyperglutamatergic, excitotoxic conditions and therefore would be devoid of such side effects. Here we report on the therapeutic effects of an orally bio-available GCP II inhibitor on established painful and sensory neuropathy in the spontaneously diabetic BB/Wor rat. It significantly improved hyperalgesia, nerve conduction velocity and underlying myelinated fiber atrophy. The data suggest that GCP II inhibition may provide a meaningful and effective approach to the treatment of painful diabetic neuropathy. |
| doi_str_mv | 10.1016/j.jns.2006.05.052 |
| format | Article |
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N-acetyl aspartyl glutamate (NAAG) by glutamate carboxypeptidase II (GCPII, also known as NAALADase). Drugs that attenuate glutamate transmission have been shown to relieve neuropathic pain, however side effects have limited their clinical use. It appears that GCPII is exclusively recruited to provide a glutamate source in hyperglutamatergic, excitotoxic conditions and therefore would be devoid of such side effects. Here we report on the therapeutic effects of an orally bio-available GCP II inhibitor on established painful and sensory neuropathy in the spontaneously diabetic BB/Wor rat. It significantly improved hyperalgesia, nerve conduction velocity and underlying myelinated fiber atrophy. The data suggest that GCP II inhibition may provide a meaningful and effective approach to the treatment of painful diabetic neuropathy.</description><identifier>ISSN: 0022-510X</identifier><identifier>EISSN: 1878-5883</identifier><identifier>DOI: 10.1016/j.jns.2006.05.052</identifier><identifier>PMID: 16780883</identifier><identifier>CODEN: JNSCAG</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Analysis of Variance ; Animals ; Associated diseases and complications ; BB/Wor rat ; Biological and medical sciences ; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction ; Diabetes. Impaired glucose tolerance ; Diabetic Neuropathies - drug therapy ; Diabetic Neuropathies - metabolism ; Diabetic Neuropathies - physiopathology ; Diabetic Neuropathies - prevention & control ; Disease Models, Animal ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Female ; GCPII inhibition ; Glutamate Carboxypeptidase II - antagonists & inhibitors ; Glutarates - therapeutic use ; Male ; Medical sciences ; Nerve Fibers, Myelinated - drug effects ; Nerve Fibers, Myelinated - pathology ; Nervous system (semeiology, syndromes) ; Neural Conduction - drug effects ; Neural Conduction - radiation effects ; Neurology ; Nociception ; Pain - drug therapy ; Pain - etiology ; Pain - metabolism ; Pain - physiopathology ; Pain Measurement - drug effects ; Rats ; Rats, Inbred BB ; Reaction Time - drug effects ; Reaction Time - physiology ; Sensory diabetic neuropathy ; Sodium-Potassium-Exchanging ATPase - metabolism ; Sulfhydryl Compounds - therapeutic use</subject><ispartof>Journal of the neurological sciences, 2006-09, Vol.247 (2), p.217-223</ispartof><rights>2006 Elsevier B.V.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-b8bd26af35c19e763f404444303a4bcd651d8dcf45f479b9b50796ce5cad5d4f3</citedby><cites>FETCH-LOGICAL-c362t-b8bd26af35c19e763f404444303a4bcd651d8dcf45f479b9b50796ce5cad5d4f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jns.2006.05.052$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18103124$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16780883$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, W.</creatorcontrib><creatorcontrib>Murakawa, Y.</creatorcontrib><creatorcontrib>Wozniak, K.M.</creatorcontrib><creatorcontrib>Slusher, B.</creatorcontrib><creatorcontrib>Sima, A.A.F.</creatorcontrib><title>The preventive and therapeutic effects of GCPII (NAALADase) inhibition on painful and sensory diabetic neuropathy</title><title>Journal of the neurological sciences</title><addtitle>J Neurol Sci</addtitle><description>Excitotoxic glutamate release occurs in several neurological disorders. One source is derived from the hydrolysis of the neuropeptide
N-acetyl aspartyl glutamate (NAAG) by glutamate carboxypeptidase II (GCPII, also known as NAALADase). Drugs that attenuate glutamate transmission have been shown to relieve neuropathic pain, however side effects have limited their clinical use. It appears that GCPII is exclusively recruited to provide a glutamate source in hyperglutamatergic, excitotoxic conditions and therefore would be devoid of such side effects. Here we report on the therapeutic effects of an orally bio-available GCP II inhibitor on established painful and sensory neuropathy in the spontaneously diabetic BB/Wor rat. It significantly improved hyperalgesia, nerve conduction velocity and underlying myelinated fiber atrophy. The data suggest that GCP II inhibition may provide a meaningful and effective approach to the treatment of painful diabetic neuropathy.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>BB/Wor rat</subject><subject>Biological and medical sciences</subject><subject>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Neuropathies - drug therapy</subject><subject>Diabetic Neuropathies - metabolism</subject><subject>Diabetic Neuropathies - physiopathology</subject><subject>Diabetic Neuropathies - prevention & control</subject><subject>Disease Models, Animal</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>GCPII inhibition</subject><subject>Glutamate Carboxypeptidase II - antagonists & inhibitors</subject><subject>Glutarates - therapeutic use</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nerve Fibers, Myelinated - drug effects</subject><subject>Nerve Fibers, Myelinated - pathology</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neural Conduction - drug effects</subject><subject>Neural Conduction - radiation effects</subject><subject>Neurology</subject><subject>Nociception</subject><subject>Pain - drug therapy</subject><subject>Pain - etiology</subject><subject>Pain - metabolism</subject><subject>Pain - physiopathology</subject><subject>Pain Measurement - drug effects</subject><subject>Rats</subject><subject>Rats, Inbred BB</subject><subject>Reaction Time - drug effects</subject><subject>Reaction Time - physiology</subject><subject>Sensory diabetic neuropathy</subject><subject>Sodium-Potassium-Exchanging ATPase - metabolism</subject><subject>Sulfhydryl Compounds - therapeutic use</subject><issn>0022-510X</issn><issn>1878-5883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFr2zAUx0XpaLN0H2CXoUvHenAmyZYt01PI2iwQth4y2E3I0hNRcGRXsgP59lOWQG99_OFdfu_P44fQZ0pmlNDy-26283HGCClnhKewKzShohIZFyK_RhNCGMs4JX9v0ccYdySBQtQ36JaWlSCJmaDXzRZwH-AAfnAHwMobPGwhqB7GwWkM1oIeIu4sXi5eViv87dd8vp7_UBEesPNb17jBdR6n9Mp5O7b_KyL42IUjNk41cOrxMIauV8P2eIc-WNVG-HTZU_Tn-Wmz-Jmtfy9Xi_k603nJhqwRjWGlsjnXtIaqzG1BijQ5yVXRaFNyaoTRtuC2qOqmbjip6lID18pwU9h8ir6ee_vQvY4QB7l3UUPbKg_dGGVSwVhVVAmkZ1CHLsYAVvbB7VU4SkrkybPcyeRZnjxLwlNYuvlyKR-bPZi3i4vYBNxfABW1am1QXrv4xglKcsqKxD2eOUgqDg6CjNqB12BcSOKl6dw7b_wD1oWbrw</recordid><startdate>20060925</startdate><enddate>20060925</enddate><creator>Zhang, W.</creator><creator>Murakawa, Y.</creator><creator>Wozniak, K.M.</creator><creator>Slusher, B.</creator><creator>Sima, A.A.F.</creator><general>Elsevier B.V</general><general>Elsevier Science</general><scope>IQODW</scope><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>20060925</creationdate><title>The preventive and therapeutic effects of GCPII (NAALADase) inhibition on painful and sensory diabetic neuropathy</title><author>Zhang, W. ; Murakawa, Y. ; Wozniak, K.M. ; Slusher, B. ; Sima, A.A.F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-b8bd26af35c19e763f404444303a4bcd651d8dcf45f479b9b50796ce5cad5d4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>BB/Wor rat</topic><topic>Biological and medical sciences</topic><topic>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Neuropathies - drug therapy</topic><topic>Diabetic Neuropathies - metabolism</topic><topic>Diabetic Neuropathies - physiopathology</topic><topic>Diabetic Neuropathies - prevention & control</topic><topic>Disease Models, Animal</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>GCPII inhibition</topic><topic>Glutamate Carboxypeptidase II - antagonists & inhibitors</topic><topic>Glutarates - therapeutic use</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nerve Fibers, Myelinated - drug effects</topic><topic>Nerve Fibers, Myelinated - pathology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neural Conduction - drug effects</topic><topic>Neural Conduction - radiation effects</topic><topic>Neurology</topic><topic>Nociception</topic><topic>Pain - drug therapy</topic><topic>Pain - etiology</topic><topic>Pain - metabolism</topic><topic>Pain - physiopathology</topic><topic>Pain Measurement - drug effects</topic><topic>Rats</topic><topic>Rats, Inbred BB</topic><topic>Reaction Time - drug effects</topic><topic>Reaction Time - physiology</topic><topic>Sensory diabetic neuropathy</topic><topic>Sodium-Potassium-Exchanging ATPase - metabolism</topic><topic>Sulfhydryl Compounds - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, W.</creatorcontrib><creatorcontrib>Murakawa, Y.</creatorcontrib><creatorcontrib>Wozniak, K.M.</creatorcontrib><creatorcontrib>Slusher, B.</creatorcontrib><creatorcontrib>Sima, A.A.F.</creatorcontrib><collection>Pascal-Francis</collection><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>Journal of the neurological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, W.</au><au>Murakawa, Y.</au><au>Wozniak, K.M.</au><au>Slusher, B.</au><au>Sima, A.A.F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The preventive and therapeutic effects of GCPII (NAALADase) inhibition on painful and sensory diabetic neuropathy</atitle><jtitle>Journal of the neurological sciences</jtitle><addtitle>J Neurol Sci</addtitle><date>2006-09-25</date><risdate>2006</risdate><volume>247</volume><issue>2</issue><spage>217</spage><epage>223</epage><pages>217-223</pages><issn>0022-510X</issn><eissn>1878-5883</eissn><coden>JNSCAG</coden><abstract>Excitotoxic glutamate release occurs in several neurological disorders. One source is derived from the hydrolysis of the neuropeptide
N-acetyl aspartyl glutamate (NAAG) by glutamate carboxypeptidase II (GCPII, also known as NAALADase). Drugs that attenuate glutamate transmission have been shown to relieve neuropathic pain, however side effects have limited their clinical use. It appears that GCPII is exclusively recruited to provide a glutamate source in hyperglutamatergic, excitotoxic conditions and therefore would be devoid of such side effects. Here we report on the therapeutic effects of an orally bio-available GCP II inhibitor on established painful and sensory neuropathy in the spontaneously diabetic BB/Wor rat. It significantly improved hyperalgesia, nerve conduction velocity and underlying myelinated fiber atrophy. The data suggest that GCP II inhibition may provide a meaningful and effective approach to the treatment of painful diabetic neuropathy.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>16780883</pmid><doi>10.1016/j.jns.2006.05.052</doi><tpages>7</tpages></addata></record> |
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| subjects | Analysis of Variance Animals Associated diseases and complications BB/Wor rat Biological and medical sciences Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction Diabetes. Impaired glucose tolerance Diabetic Neuropathies - drug therapy Diabetic Neuropathies - metabolism Diabetic Neuropathies - physiopathology Diabetic Neuropathies - prevention & control Disease Models, Animal Endocrine pancreas. Apud cells (diseases) Endocrinopathies Female GCPII inhibition Glutamate Carboxypeptidase II - antagonists & inhibitors Glutarates - therapeutic use Male Medical sciences Nerve Fibers, Myelinated - drug effects Nerve Fibers, Myelinated - pathology Nervous system (semeiology, syndromes) Neural Conduction - drug effects Neural Conduction - radiation effects Neurology Nociception Pain - drug therapy Pain - etiology Pain - metabolism Pain - physiopathology Pain Measurement - drug effects Rats Rats, Inbred BB Reaction Time - drug effects Reaction Time - physiology Sensory diabetic neuropathy Sodium-Potassium-Exchanging ATPase - metabolism Sulfhydryl Compounds - therapeutic use |
| title | The preventive and therapeutic effects of GCPII (NAALADase) inhibition on painful and sensory diabetic neuropathy |
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