Neuropharmacological profile of a selective sigma ligand, igmesine: a potential antidepressant
Igmesine is a selective sigma (σ 1) ligand that was reported to exert antidepressant action through an unknown mechanism of action. A number of neurochemical measures were taken in this study in efforts to understand its mode of action. Following 21-day drug treatments, the actions of igmesine on a...
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| description | Igmesine is a selective sigma (σ
1) ligand that was reported to exert antidepressant action through an unknown mechanism of action. A number of neurochemical measures were taken in this study in efforts to understand its mode of action. Following 21-day drug treatments, the actions of igmesine on a number of neurochemical measures were investigated. Data obtained showed significant decreases in the densities of β-adrenergic but not 5-HT
1A, σ
1 and GABA
B receptors in fluoxetine (18%), desipramine (DMI, 32%) and igmesine (20%)-treated groups when compared with control. Tyrosine hydroxylase (TH) activity was significantly (30–32%) reduced in all treated groups. Further, fluoxetine and DMI excluding the igmesine-treated groups showed 85 and 40% reductions in serotonin (5-HT) and noradrenaline (NE) neuronal uptake, respectively. Following acute treatment, igmesine lacked activity for monoamine oxidase (MAO) A or B (IC
50>10
μM). In in vivo studies, at behaviorally active doses, igmesine showed weak effects on the NE uptake but lacked activity in altering 5-HT and DA synthesis or antagonizing selective drug-induced depletion of monoamine neuronal uptake.
N-methyl-
d-aspartate (NMDA)-induced increases in cGMP was blocked by igmesine indicating that igmesine may interfere with the NMDA receptor/nitric oxide synthase/cGMP pathway. Although it appears that part of the pharmacological actions of igmesine is mediated by the monoaminergic system, there is still need to explore other possible mechanisms of antidepressant action. |
| doi_str_mv | 10.1016/S0028-3908(01)00049-1 |
| format | Article |
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1) ligand that was reported to exert antidepressant action through an unknown mechanism of action. A number of neurochemical measures were taken in this study in efforts to understand its mode of action. Following 21-day drug treatments, the actions of igmesine on a number of neurochemical measures were investigated. Data obtained showed significant decreases in the densities of β-adrenergic but not 5-HT
1A, σ
1 and GABA
B receptors in fluoxetine (18%), desipramine (DMI, 32%) and igmesine (20%)-treated groups when compared with control. Tyrosine hydroxylase (TH) activity was significantly (30–32%) reduced in all treated groups. Further, fluoxetine and DMI excluding the igmesine-treated groups showed 85 and 40% reductions in serotonin (5-HT) and noradrenaline (NE) neuronal uptake, respectively. Following acute treatment, igmesine lacked activity for monoamine oxidase (MAO) A or B (IC
50>10
μM). In in vivo studies, at behaviorally active doses, igmesine showed weak effects on the NE uptake but lacked activity in altering 5-HT and DA synthesis or antagonizing selective drug-induced depletion of monoamine neuronal uptake.
N-methyl-
d-aspartate (NMDA)-induced increases in cGMP was blocked by igmesine indicating that igmesine may interfere with the NMDA receptor/nitric oxide synthase/cGMP pathway. Although it appears that part of the pharmacological actions of igmesine is mediated by the monoaminergic system, there is still need to explore other possible mechanisms of antidepressant action.</description><identifier>ISSN: 0028-3908</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/S0028-3908(01)00049-1</identifier><identifier>PMID: 11445194</identifier><identifier>CODEN: NEPHBW</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Adrenergic alpha-Agonists - pharmacology ; Animals ; Antidepressive Agents - pharmacology ; b-Adrenergic receptors ; Biogenic Monoamines - metabolism ; Biological and medical sciences ; Brain Chemistry - drug effects ; cGMP ; Chromatography, High Pressure Liquid ; Cinnamates - pharmacology ; Cyclic AMP - metabolism ; Cyclopropanes - pharmacology ; Dissociation constant ; Idazoxan - pharmacology ; igmesine ; Male ; Medical sciences ; Monoamine oxidase ; Monoamine Oxidase - metabolism ; N-Methyl- d-aspartate ; N-Methyl-D-aspartic acid ; Neuronal uptake ; Neurons - drug effects ; Neurons - metabolism ; Neuropharmacology ; Nitric oxide synthase ; Pharmacology. Drug treatments ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopharmacology ; Radioligand Assay ; Rats ; Rats, Sprague-Dawley ; Receptor density ; Receptors, Adrenergic, beta - drug effects ; Receptors, Adrenergic, beta - metabolism ; Receptors, GABA-B - metabolism ; Receptors, Serotonin - drug effects ; Receptors, Serotonin, 5-HT1 ; Receptors, sigma - drug effects ; Sigma binding site ; Synaptosome ; Synaptosomes - drug effects ; Synaptosomes - metabolism ; Tyrosine 3-Monooxygenase - metabolism ; Tyrosine hydroxylase</subject><ispartof>Neuropharmacology, 2001-07, Vol.41 (1), p.138-149</ispartof><rights>2001 Elsevier Science Ltd</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-aee63984e8139c8fac46b01271f80c34afd80144003c5009163b9e82e28392173</citedby><cites>FETCH-LOGICAL-c421t-aee63984e8139c8fac46b01271f80c34afd80144003c5009163b9e82e28392173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0028390801000491$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1068154$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11445194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Akunne, H.C</creatorcontrib><creatorcontrib>Zoski, K.T</creatorcontrib><creatorcontrib>Whetzel, S.Z</creatorcontrib><creatorcontrib>Cordon, J.J</creatorcontrib><creatorcontrib>Brandon, R.M</creatorcontrib><creatorcontrib>Roman, F</creatorcontrib><creatorcontrib>Pugsley, T.A</creatorcontrib><title>Neuropharmacological profile of a selective sigma ligand, igmesine: a potential antidepressant</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>Igmesine is a selective sigma (σ
1) ligand that was reported to exert antidepressant action through an unknown mechanism of action. A number of neurochemical measures were taken in this study in efforts to understand its mode of action. Following 21-day drug treatments, the actions of igmesine on a number of neurochemical measures were investigated. Data obtained showed significant decreases in the densities of β-adrenergic but not 5-HT
1A, σ
1 and GABA
B receptors in fluoxetine (18%), desipramine (DMI, 32%) and igmesine (20%)-treated groups when compared with control. Tyrosine hydroxylase (TH) activity was significantly (30–32%) reduced in all treated groups. Further, fluoxetine and DMI excluding the igmesine-treated groups showed 85 and 40% reductions in serotonin (5-HT) and noradrenaline (NE) neuronal uptake, respectively. Following acute treatment, igmesine lacked activity for monoamine oxidase (MAO) A or B (IC
50>10
μM). In in vivo studies, at behaviorally active doses, igmesine showed weak effects on the NE uptake but lacked activity in altering 5-HT and DA synthesis or antagonizing selective drug-induced depletion of monoamine neuronal uptake.
N-methyl-
d-aspartate (NMDA)-induced increases in cGMP was blocked by igmesine indicating that igmesine may interfere with the NMDA receptor/nitric oxide synthase/cGMP pathway. Although it appears that part of the pharmacological actions of igmesine is mediated by the monoaminergic system, there is still need to explore other possible mechanisms of antidepressant action.</description><subject>Adrenergic alpha-Agonists - pharmacology</subject><subject>Animals</subject><subject>Antidepressive Agents - pharmacology</subject><subject>b-Adrenergic receptors</subject><subject>Biogenic Monoamines - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain Chemistry - drug effects</subject><subject>cGMP</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Cinnamates - pharmacology</subject><subject>Cyclic AMP - metabolism</subject><subject>Cyclopropanes - pharmacology</subject><subject>Dissociation constant</subject><subject>Idazoxan - pharmacology</subject><subject>igmesine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Monoamine oxidase</subject><subject>Monoamine Oxidase - metabolism</subject><subject>N-Methyl- d-aspartate</subject><subject>N-Methyl-D-aspartic acid</subject><subject>Neuronal uptake</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuropharmacology</subject><subject>Nitric oxide synthase</subject><subject>Pharmacology. Drug treatments</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Radioligand Assay</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor density</subject><subject>Receptors, Adrenergic, beta - drug effects</subject><subject>Receptors, Adrenergic, beta - metabolism</subject><subject>Receptors, GABA-B - metabolism</subject><subject>Receptors, Serotonin - drug effects</subject><subject>Receptors, Serotonin, 5-HT1</subject><subject>Receptors, sigma - drug effects</subject><subject>Sigma binding site</subject><subject>Synaptosome</subject><subject>Synaptosomes - drug effects</subject><subject>Synaptosomes - metabolism</subject><subject>Tyrosine 3-Monooxygenase - metabolism</subject><subject>Tyrosine hydroxylase</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9P3DAQxS1U1N1CP0KrHCpUJAIzsZM4XFCF-CchONBesbzOZGuUxMFOkPj29bKrwm1PM5Z-b_z0HmPfEI4RsDh5AMhkyiuQPwEPAUBUKe6wOcqSpyUU4hOb_0dm7EsITytIovzMZohC5FiJOXu8o8m74a_2nTaudUtrdJsM3jW2pcQ1iU4CtWRG-0JJsMtOJ61d6r4-SuKDgu3pNDKDG6kfbZTqOGoaPIUQ13222-g20NfN3GN_Li9-n1-nt_dXN-e_blMjMhxTTVTwSgqSyCsjG21EsQDMSmwkGC50U0uIngG4yQEqLPiiIplRJnmVYcn32MH6bnT-PFEYVWeDobbVPbkpqBIBCsz5VhBjQCVKGcF8DRrvQvDUqMHbTvtXhaBWDai3BtQqXgWo3hpQGHXfNx9Mi47qd9Um8gj82AA6xKwbr3tjw4frhcR8hZ2tMYqxvVjyKhhLvaHa-liHqp3d4uQfR5ihkg</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>Akunne, H.C</creator><creator>Zoski, K.T</creator><creator>Whetzel, S.Z</creator><creator>Cordon, J.J</creator><creator>Brandon, R.M</creator><creator>Roman, F</creator><creator>Pugsley, T.A</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><scope>7X8</scope></search><sort><creationdate>20010701</creationdate><title>Neuropharmacological profile of a selective sigma ligand, igmesine: a potential antidepressant</title><author>Akunne, H.C ; Zoski, K.T ; Whetzel, S.Z ; Cordon, J.J ; Brandon, R.M ; Roman, F ; Pugsley, T.A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-aee63984e8139c8fac46b01271f80c34afd80144003c5009163b9e82e28392173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adrenergic alpha-Agonists - pharmacology</topic><topic>Animals</topic><topic>Antidepressive Agents - pharmacology</topic><topic>b-Adrenergic receptors</topic><topic>Biogenic Monoamines - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain Chemistry - drug effects</topic><topic>cGMP</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Cinnamates - pharmacology</topic><topic>Cyclic AMP - metabolism</topic><topic>Cyclopropanes - pharmacology</topic><topic>Dissociation constant</topic><topic>Idazoxan - pharmacology</topic><topic>igmesine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Monoamine oxidase</topic><topic>Monoamine Oxidase - metabolism</topic><topic>N-Methyl- d-aspartate</topic><topic>N-Methyl-D-aspartic acid</topic><topic>Neuronal uptake</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuropharmacology</topic><topic>Nitric oxide synthase</topic><topic>Pharmacology. Drug treatments</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Radioligand Assay</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor density</topic><topic>Receptors, Adrenergic, beta - drug effects</topic><topic>Receptors, Adrenergic, beta - metabolism</topic><topic>Receptors, GABA-B - metabolism</topic><topic>Receptors, Serotonin - drug effects</topic><topic>Receptors, Serotonin, 5-HT1</topic><topic>Receptors, sigma - drug effects</topic><topic>Sigma binding site</topic><topic>Synaptosome</topic><topic>Synaptosomes - drug effects</topic><topic>Synaptosomes - metabolism</topic><topic>Tyrosine 3-Monooxygenase - metabolism</topic><topic>Tyrosine hydroxylase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Akunne, H.C</creatorcontrib><creatorcontrib>Zoski, K.T</creatorcontrib><creatorcontrib>Whetzel, S.Z</creatorcontrib><creatorcontrib>Cordon, J.J</creatorcontrib><creatorcontrib>Brandon, R.M</creatorcontrib><creatorcontrib>Roman, F</creatorcontrib><creatorcontrib>Pugsley, T.A</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><collection>MEDLINE - Academic</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Akunne, H.C</au><au>Zoski, K.T</au><au>Whetzel, S.Z</au><au>Cordon, J.J</au><au>Brandon, R.M</au><au>Roman, F</au><au>Pugsley, T.A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuropharmacological profile of a selective sigma ligand, igmesine: a potential antidepressant</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>2001-07-01</date><risdate>2001</risdate><volume>41</volume><issue>1</issue><spage>138</spage><epage>149</epage><pages>138-149</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><coden>NEPHBW</coden><abstract>Igmesine is a selective sigma (σ
1) ligand that was reported to exert antidepressant action through an unknown mechanism of action. A number of neurochemical measures were taken in this study in efforts to understand its mode of action. Following 21-day drug treatments, the actions of igmesine on a number of neurochemical measures were investigated. Data obtained showed significant decreases in the densities of β-adrenergic but not 5-HT
1A, σ
1 and GABA
B receptors in fluoxetine (18%), desipramine (DMI, 32%) and igmesine (20%)-treated groups when compared with control. Tyrosine hydroxylase (TH) activity was significantly (30–32%) reduced in all treated groups. Further, fluoxetine and DMI excluding the igmesine-treated groups showed 85 and 40% reductions in serotonin (5-HT) and noradrenaline (NE) neuronal uptake, respectively. Following acute treatment, igmesine lacked activity for monoamine oxidase (MAO) A or B (IC
50>10
μM). In in vivo studies, at behaviorally active doses, igmesine showed weak effects on the NE uptake but lacked activity in altering 5-HT and DA synthesis or antagonizing selective drug-induced depletion of monoamine neuronal uptake.
N-methyl-
d-aspartate (NMDA)-induced increases in cGMP was blocked by igmesine indicating that igmesine may interfere with the NMDA receptor/nitric oxide synthase/cGMP pathway. Although it appears that part of the pharmacological actions of igmesine is mediated by the monoaminergic system, there is still need to explore other possible mechanisms of antidepressant action.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>11445194</pmid><doi>10.1016/S0028-3908(01)00049-1</doi><tpages>12</tpages></addata></record> |
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| subjects | Adrenergic alpha-Agonists - pharmacology Animals Antidepressive Agents - pharmacology b-Adrenergic receptors Biogenic Monoamines - metabolism Biological and medical sciences Brain Chemistry - drug effects cGMP Chromatography, High Pressure Liquid Cinnamates - pharmacology Cyclic AMP - metabolism Cyclopropanes - pharmacology Dissociation constant Idazoxan - pharmacology igmesine Male Medical sciences Monoamine oxidase Monoamine Oxidase - metabolism N-Methyl- d-aspartate N-Methyl-D-aspartic acid Neuronal uptake Neurons - drug effects Neurons - metabolism Neuropharmacology Nitric oxide synthase Pharmacology. Drug treatments Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopharmacology Radioligand Assay Rats Rats, Sprague-Dawley Receptor density Receptors, Adrenergic, beta - drug effects Receptors, Adrenergic, beta - metabolism Receptors, GABA-B - metabolism Receptors, Serotonin - drug effects Receptors, Serotonin, 5-HT1 Receptors, sigma - drug effects Sigma binding site Synaptosome Synaptosomes - drug effects Synaptosomes - metabolism Tyrosine 3-Monooxygenase - metabolism Tyrosine hydroxylase |
| title | Neuropharmacological profile of a selective sigma ligand, igmesine: a potential antidepressant |
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