The peroxynitrite donor 3-morpholinosydnonimine induces reversible changes in electrophysiological properties of neurons of the guinea-pig spinal cord
Abstract Elevated concentrations of nitric oxide (NO) and peroxynitrite (ONOO− ) are present within the CNS following neurotrauma and are implicated in the pathogenesis of the accompanying neurologic deficits. We tested the hypothesis that elevated extracellular concentrations of ONOO− , introduced...
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| Veröffentlicht in: | Neuroscience 2008-09, Vol.156 (1), p.107-117 |
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| description | Abstract Elevated concentrations of nitric oxide (NO) and peroxynitrite (ONOO− ) are present within the CNS following neurotrauma and are implicated in the pathogenesis of the accompanying neurologic deficits. We tested the hypothesis that elevated extracellular concentrations of ONOO− , introduced by the donor 3-morpholinosydnonimine (SIN-1), induce reversible axonal conduction deficits in neurons of the guinea-pig spinal cord. The compound action potential (CAP) and compound membrane potential (CMP) of excised ventral cord white matter were recorded before, during, and after, bathing the tissue (30 min) in varying concentrations (0.125–2.0 mM) of SIN-1 ( 3.75–60 μM ONOO− ). The principal results were rapid onset, concentration-dependent, reductions in amplitude of the CAP ( P |
| doi_str_mv | 10.1016/j.neuroscience.2008.06.050 |
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We tested the hypothesis that elevated extracellular concentrations of ONOO− , introduced by the donor 3-morpholinosydnonimine (SIN-1), induce reversible axonal conduction deficits in neurons of the guinea-pig spinal cord. The compound action potential (CAP) and compound membrane potential (CMP) of excised ventral cord white matter were recorded before, during, and after, bathing the tissue (30 min) in varying concentrations (0.125–2.0 mM) of SIN-1 ( 3.75–60 μM ONOO− ). The principal results were rapid onset, concentration-dependent, reductions in amplitude of the CAP ( P <0.05). At a concentration of 0.25 mM of SIN-1 the reduction in CAP amplitude was fully reversible and was not accompanied by any changes in CMP. At higher concentrations of SIN-1 (≥0.5 mM) the reversibility was incomplete and there was concurrent depolarization of the CMP. These electrophysiological changes were not evident when the donor had been a priori depleted of ONOO− by uric acid or was co-administered with the ONOO− scavenger ebselen (3 mM). Immuno-fluorescence staining for nitrotyrosine (Ntyr) revealed extensive nitration of tyrosine residues in neurons exposed to higher concentrations of SIN-1. These results are the first to demonstrate that ONOO− induces reversible conduction deficits within axons of the spinal cord. The dissociation of CAP and CMP changes at low concentrations of SIN-1, when the CAP changes were reversible and there was no evidence of nitration of tyrosine residues, is consistent with ONOO− -induced alteration in Na+ channel conductance in the axolemma. The results support the view that ONOO− contributes to both reversible and non-reversible neurologic deficits following neurotrauma. The reversal of immune-mediated conduction deficits may contribute to spontaneous neurologic deficits following neurotrauma.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/j.neuroscience.2008.06.050</identifier><identifier>PMID: 18662749</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Action Potentials - drug effects ; Action Potentials - physiology ; Animals ; axons ; Axons - drug effects ; Axons - metabolism ; Biological and medical sciences ; Cell Membrane - drug effects ; Cell Membrane - metabolism ; conduction ; Dose-Response Relationship, Drug ; Extracellular Fluid - drug effects ; Extracellular Fluid - metabolism ; Female ; Fundamental and applied biological sciences. Psychology ; Guinea Pigs ; immuno-fluorescence ; Molsidomine - analogs & derivatives ; Molsidomine - toxicity ; Nerve Degeneration - chemically induced ; Nerve Degeneration - metabolism ; Nerve Degeneration - physiopathology ; Neural Conduction - drug effects ; Neural Conduction - physiology ; Neurology ; Neurons - drug effects ; Neurons - metabolism ; Neurons - physiology ; neurotrauma ; nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Donors - toxicity ; Nitro Compounds - metabolism ; Peroxynitrous Acid - agonists ; Peroxynitrous Acid - metabolism ; Peroxynitrous Acid - toxicity ; Sodium Channels - drug effects ; Sodium Channels - metabolism ; Spinal Cord - drug effects ; Spinal Cord - metabolism ; Spinal Cord - physiopathology ; Spinal Cord Injuries - drug therapy ; Spinal Cord Injuries - metabolism ; Spinal Cord Injuries - physiopathology ; spinal cord injury ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 2008-09, Vol.156 (1), p.107-117</ispartof><rights>IBRO</rights><rights>2008 IBRO</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-bac6b14a0870ce7bee1bad04709f4c2a2e9d15580dbf03cf88f01bf053e272e63</citedby><cites>FETCH-LOGICAL-c494t-bac6b14a0870ce7bee1bad04709f4c2a2e9d15580dbf03cf88f01bf053e272e63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0306452208009007$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20697798$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18662749$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ashki, N</creatorcontrib><creatorcontrib>Hayes, K.C</creatorcontrib><creatorcontrib>Bao, F</creatorcontrib><title>The peroxynitrite donor 3-morpholinosydnonimine induces reversible changes in electrophysiological properties of neurons of the guinea-pig spinal cord</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Abstract Elevated concentrations of nitric oxide (NO) and peroxynitrite (ONOO− ) are present within the CNS following neurotrauma and are implicated in the pathogenesis of the accompanying neurologic deficits. We tested the hypothesis that elevated extracellular concentrations of ONOO− , introduced by the donor 3-morpholinosydnonimine (SIN-1), induce reversible axonal conduction deficits in neurons of the guinea-pig spinal cord. The compound action potential (CAP) and compound membrane potential (CMP) of excised ventral cord white matter were recorded before, during, and after, bathing the tissue (30 min) in varying concentrations (0.125–2.0 mM) of SIN-1 ( 3.75–60 μM ONOO− ). The principal results were rapid onset, concentration-dependent, reductions in amplitude of the CAP ( P <0.05). At a concentration of 0.25 mM of SIN-1 the reduction in CAP amplitude was fully reversible and was not accompanied by any changes in CMP. At higher concentrations of SIN-1 (≥0.5 mM) the reversibility was incomplete and there was concurrent depolarization of the CMP. These electrophysiological changes were not evident when the donor had been a priori depleted of ONOO− by uric acid or was co-administered with the ONOO− scavenger ebselen (3 mM). Immuno-fluorescence staining for nitrotyrosine (Ntyr) revealed extensive nitration of tyrosine residues in neurons exposed to higher concentrations of SIN-1. These results are the first to demonstrate that ONOO− induces reversible conduction deficits within axons of the spinal cord. The dissociation of CAP and CMP changes at low concentrations of SIN-1, when the CAP changes were reversible and there was no evidence of nitration of tyrosine residues, is consistent with ONOO− -induced alteration in Na+ channel conductance in the axolemma. The results support the view that ONOO− contributes to both reversible and non-reversible neurologic deficits following neurotrauma. The reversal of immune-mediated conduction deficits may contribute to spontaneous neurologic deficits following neurotrauma.</description><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>axons</subject><subject>Axons - drug effects</subject><subject>Axons - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - metabolism</subject><subject>conduction</subject><subject>Dose-Response Relationship, Drug</subject><subject>Extracellular Fluid - drug effects</subject><subject>Extracellular Fluid - metabolism</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guinea Pigs</subject><subject>immuno-fluorescence</subject><subject>Molsidomine - analogs & derivatives</subject><subject>Molsidomine - toxicity</subject><subject>Nerve Degeneration - chemically induced</subject><subject>Nerve Degeneration - metabolism</subject><subject>Nerve Degeneration - physiopathology</subject><subject>Neural Conduction - drug effects</subject><subject>Neural Conduction - physiology</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>neurotrauma</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Donors - toxicity</subject><subject>Nitro Compounds - metabolism</subject><subject>Peroxynitrous Acid - agonists</subject><subject>Peroxynitrous Acid - metabolism</subject><subject>Peroxynitrous Acid - toxicity</subject><subject>Sodium Channels - drug effects</subject><subject>Sodium Channels - metabolism</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - physiopathology</subject><subject>Spinal Cord Injuries - drug therapy</subject><subject>Spinal Cord Injuries - metabolism</subject><subject>Spinal Cord Injuries - physiopathology</subject><subject>spinal cord injury</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkl2L1TAQhoMo7nH1L0gR9K51kqZN64Ug6ycseOF6HdJkek6OPUlN2sX-EX-v6Z6i4pW5yTA888H7DiHPKBQUaP3yWDicg4_aotNYMICmgLqACu6RHW1EmYuK8_tkByXUOa8YuyCPYjxCehUvH5IL2tQ1E7zdkZ83B8xGDP7H4uwU7ISZ8c6HrMxPPowHP1jn42Kcd_ZkHWbWmVljzALeYoi2GzDTB-X2KWVdhgPqKfjxsETrB7-3Wg3ZmBIYJpsQ32d3u7u7cEqz93PqqvLR7rM4Wpdw7YN5TB70aoj4ZPsvydf3726uPubXnz98unpznWve8invlK47yhU0AjSKDpF2ygAX0PZcM8WwNbSqGjBdD6Xum6YHmsKqRCYY1uUleXHum3b8PmOc5MlGjcOgHPo5SgatKIGv4KszqJPwMWAvx2BPKiySglxdkUf5tytydUVCLZMrqfjpNmXuTmj-lG42JOD5BqiYFOuDctrG3xyDuhWibRL39sxh0uTWYpDbOGNDEl4ab_9vn9f_tNHJ5tWrb7hgPPo5JCOipDIyCfLLekfrGUED0AKI8hcvPsyX</recordid><startdate>20080922</startdate><enddate>20080922</enddate><creator>Ashki, N</creator><creator>Hayes, K.C</creator><creator>Bao, F</creator><general>Elsevier Ltd</general><general>Elsevier</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>7TK</scope></search><sort><creationdate>20080922</creationdate><title>The peroxynitrite donor 3-morpholinosydnonimine induces reversible changes in electrophysiological properties of neurons of the guinea-pig spinal cord</title><author>Ashki, N ; Hayes, K.C ; Bao, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-bac6b14a0870ce7bee1bad04709f4c2a2e9d15580dbf03cf88f01bf053e272e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Animals</topic><topic>axons</topic><topic>Axons - drug effects</topic><topic>Axons - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell Membrane - drug effects</topic><topic>Cell Membrane - metabolism</topic><topic>conduction</topic><topic>Dose-Response Relationship, Drug</topic><topic>Extracellular Fluid - drug effects</topic><topic>Extracellular Fluid - metabolism</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guinea Pigs</topic><topic>immuno-fluorescence</topic><topic>Molsidomine - analogs & derivatives</topic><topic>Molsidomine - toxicity</topic><topic>Nerve Degeneration - chemically induced</topic><topic>Nerve Degeneration - metabolism</topic><topic>Nerve Degeneration - physiopathology</topic><topic>Neural Conduction - drug effects</topic><topic>Neural Conduction - physiology</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>neurotrauma</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Donors - toxicity</topic><topic>Nitro Compounds - metabolism</topic><topic>Peroxynitrous Acid - agonists</topic><topic>Peroxynitrous Acid - metabolism</topic><topic>Peroxynitrous Acid - toxicity</topic><topic>Sodium Channels - drug effects</topic><topic>Sodium Channels - metabolism</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - physiopathology</topic><topic>Spinal Cord Injuries - drug therapy</topic><topic>Spinal Cord Injuries - metabolism</topic><topic>Spinal Cord Injuries - physiopathology</topic><topic>spinal cord injury</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ashki, N</creatorcontrib><creatorcontrib>Hayes, K.C</creatorcontrib><creatorcontrib>Bao, 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>Neurosciences Abstracts</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ashki, N</au><au>Hayes, K.C</au><au>Bao, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The peroxynitrite donor 3-morpholinosydnonimine induces reversible changes in electrophysiological properties of neurons of the guinea-pig spinal cord</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2008-09-22</date><risdate>2008</risdate><volume>156</volume><issue>1</issue><spage>107</spage><epage>117</epage><pages>107-117</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Abstract Elevated concentrations of nitric oxide (NO) and peroxynitrite (ONOO− ) are present within the CNS following neurotrauma and are implicated in the pathogenesis of the accompanying neurologic deficits. We tested the hypothesis that elevated extracellular concentrations of ONOO− , introduced by the donor 3-morpholinosydnonimine (SIN-1), induce reversible axonal conduction deficits in neurons of the guinea-pig spinal cord. The compound action potential (CAP) and compound membrane potential (CMP) of excised ventral cord white matter were recorded before, during, and after, bathing the tissue (30 min) in varying concentrations (0.125–2.0 mM) of SIN-1 ( 3.75–60 μM ONOO− ). The principal results were rapid onset, concentration-dependent, reductions in amplitude of the CAP ( P <0.05). At a concentration of 0.25 mM of SIN-1 the reduction in CAP amplitude was fully reversible and was not accompanied by any changes in CMP. At higher concentrations of SIN-1 (≥0.5 mM) the reversibility was incomplete and there was concurrent depolarization of the CMP. These electrophysiological changes were not evident when the donor had been a priori depleted of ONOO− by uric acid or was co-administered with the ONOO− scavenger ebselen (3 mM). Immuno-fluorescence staining for nitrotyrosine (Ntyr) revealed extensive nitration of tyrosine residues in neurons exposed to higher concentrations of SIN-1. These results are the first to demonstrate that ONOO− induces reversible conduction deficits within axons of the spinal cord. The dissociation of CAP and CMP changes at low concentrations of SIN-1, when the CAP changes were reversible and there was no evidence of nitration of tyrosine residues, is consistent with ONOO− -induced alteration in Na+ channel conductance in the axolemma. The results support the view that ONOO− contributes to both reversible and non-reversible neurologic deficits following neurotrauma. The reversal of immune-mediated conduction deficits may contribute to spontaneous neurologic deficits following neurotrauma.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>18662749</pmid><doi>10.1016/j.neuroscience.2008.06.050</doi><tpages>11</tpages></addata></record> |
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| subjects | Action Potentials - drug effects Action Potentials - physiology Animals axons Axons - drug effects Axons - metabolism Biological and medical sciences Cell Membrane - drug effects Cell Membrane - metabolism conduction Dose-Response Relationship, Drug Extracellular Fluid - drug effects Extracellular Fluid - metabolism Female Fundamental and applied biological sciences. Psychology Guinea Pigs immuno-fluorescence Molsidomine - analogs & derivatives Molsidomine - toxicity Nerve Degeneration - chemically induced Nerve Degeneration - metabolism Nerve Degeneration - physiopathology Neural Conduction - drug effects Neural Conduction - physiology Neurology Neurons - drug effects Neurons - metabolism Neurons - physiology neurotrauma nitric oxide Nitric Oxide - metabolism Nitric Oxide Donors - toxicity Nitro Compounds - metabolism Peroxynitrous Acid - agonists Peroxynitrous Acid - metabolism Peroxynitrous Acid - toxicity Sodium Channels - drug effects Sodium Channels - metabolism Spinal Cord - drug effects Spinal Cord - metabolism Spinal Cord - physiopathology Spinal Cord Injuries - drug therapy Spinal Cord Injuries - metabolism Spinal Cord Injuries - physiopathology spinal cord injury Tyrosine - analogs & derivatives Tyrosine - metabolism Vertebrates: nervous system and sense organs |
| title | The peroxynitrite donor 3-morpholinosydnonimine induces reversible changes in electrophysiological properties of neurons of the guinea-pig spinal cord |
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