DOPA causes glutamate release and delayed neuron death by brain ischemia in rats
Identifieur interne : 001021 ( PascalFrancis/Corpus ); précédent : 001020; suivant : 001022DOPA causes glutamate release and delayed neuron death by brain ischemia in rats
Auteurs : Yoshimi Misu ; Nobuya Furukawa ; Nobutaka Arai ; Takeaki Miyamae ; Yoshio Goshima ; Kiyohide FujitaSource :
- Neurotoxicology and teratology [ 0892-0362 ] ; 2002.
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Abstract
DOPA seems to be a neuromodulator in striata and hippocampal CAI and a neurotransmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS) and baroreflex pathways in the caudal ventrolateral medulla and rostral ventrolateral medulla in the brainstem of rats. DOPA recognition sites differ from dopamine (DA) D1 and D2 and ionotropic glutamate receptors. Via DOPA sites, DOPA stereoselectively releases by itself neuronal glutamate from in vitro and in vivo striata. In the cultured neurons, DOPA and DA cause neuron death via autoxidation. In addition, DOPA causes autoxidation-irrelevant neuron death via glutamate release. Furthermore, DOPA released by four-vessel occlusion seems to be an upstream causal factor for glutamate release and resultant delayed neuron death by brain ischemia in striata and hippocampal CA1. Glutamate has been regarded as a neurotransmitter of baroreflex pathways. Herein, we propose a new pathway that DOPA is a neurotransmitter of the primary aortic depressor nerve and glutamate is that of secondary neurons in neuronal microcircuits of'depressor sites in the NTS. DOPA seems to release unmeasurable, but functioning, endogenous glutamate from the secondary neurons via DOPA sites. A common following pathway may be ionotropic glutamate receptors-nNOS activation-NO production-baroreflex neurotransmission and delayed neuron death. However, we are concerned that DOPA therapy may accelerate neuronal degeneration process especially at progressive stages of Parkinson's disease.
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Format Inist (serveur)
| NO : | PASCAL 03-0018077 INIST |
|---|---|
| ET : | DOPA causes glutamate release and delayed neuron death by brain ischemia in rats |
| AU : | MISU (Yoshimi); FURUKAWA (Nobuya); ARAI (Nobutaka); MIYAMAE (Takeaki); GOSHIMA (Yoshio); FUJITA (Kiyohide); NAOI (Makoto); PARVEZ (Hasan); MARUYAMA (Wakako); COLLINS (Michel A.); YOUDIM (Moussa B. H.) |
| AF : | Department of Pharmacology, Yokohama City University School of Medicine/Yokohama 236-0004/Japon (1 aut., 2 aut., 4 aut., 5 aut.); Shinobu Hospital/Fukushima 960-1101/Japon (1 aut.); Department of Oral and Maxillofacial Surgery, Yokohama City University School of Medicine/Yokohama 236-0004/Japon (2 aut., 6 aut.); Department of Clinical Neuropathology, Tokyo Metropolitan Institute of Neuroscience/Tokyo 183-8526/Japon (3 aut.); Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park/Mitake, Gifu 505-0116/Japon (1 aut.); Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut.); Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences/Obu, Aichi 474-8622/Japon (3 aut.); Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine/Maywood, IL 60153/Etats-Unis (4 aut.); Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion/Haifa 31096/Israël (5 aut.) |
| DT : | Publication en série; Congrès; Niveau analytique |
| SO : | Neurotoxicology and teratology; ISSN 0892-0362; Coden NETEEC; Etats-Unis; Da. 2002; Vol. 24; No. 5; Pp. 629-638; Bibl. 60 ref. |
| LA : | Anglais |
| EA : | DOPA seems to be a neuromodulator in striata and hippocampal CAI and a neurotransmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS) and baroreflex pathways in the caudal ventrolateral medulla and rostral ventrolateral medulla in the brainstem of rats. DOPA recognition sites differ from dopamine (DA) D1 and D2 and ionotropic glutamate receptors. Via DOPA sites, DOPA stereoselectively releases by itself neuronal glutamate from in vitro and in vivo striata. In the cultured neurons, DOPA and DA cause neuron death via autoxidation. In addition, DOPA causes autoxidation-irrelevant neuron death via glutamate release. Furthermore, DOPA released by four-vessel occlusion seems to be an upstream causal factor for glutamate release and resultant delayed neuron death by brain ischemia in striata and hippocampal CA1. Glutamate has been regarded as a neurotransmitter of baroreflex pathways. Herein, we propose a new pathway that DOPA is a neurotransmitter of the primary aortic depressor nerve and glutamate is that of secondary neurons in neuronal microcircuits of'depressor sites in the NTS. DOPA seems to release unmeasurable, but functioning, endogenous glutamate from the secondary neurons via DOPA sites. A common following pathway may be ionotropic glutamate receptors-nNOS activation-NO production-baroreflex neurotransmission and delayed neuron death. However, we are concerned that DOPA therapy may accelerate neuronal degeneration process especially at progressive stages of Parkinson's disease. |
| CC : | 002B17G; 002B02B06 |
| FD : | Lévodopa; In vitro; In vivo; Rat; Animal; Traitement; Parkinson maladie; Chimiothérapie; Toxicité; Corps strié; Mécanisme action; Stade clinique; Progressif |
| FG : | Rodentia; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative |
| ED : | Levodopa; In vitro; In vivo; Rat; Animal; Treatment; Parkinson disease; Chemotherapy; Toxicity; Corpus striatum; Mechanism of action; Clinical stage; Progressive |
| EG : | Rodentia; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease |
| SD : | Levodopa; In vitro; In vivo; Rata; Animal; Tratamiento; Parkinson enfermedad; Quimioterapia; Toxicidad; Cuerpo estriado; Mecanismo acción; Estadio clínico; Progresivo |
| LO : | INIST-18910.354000109244300080 |
| ID : | 03-0018077 |
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Pascal:03-0018077Le document en format XML
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University School of Medicine</s1><s2>Yokohama 236-0004</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Department of Oral and Maxillofacial Surgery, Yokohama City University School of Medicine</s1><s2>Yokohama 236-0004</s2><s3>JPN</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Arai, Nobutaka" sort="Arai, Nobutaka" uniqKey="Arai N" first="Nobutaka" last="Arai">Nobutaka Arai</name><affiliation><inist:fA14 i1="04"><s1>Department of Clinical Neuropathology, Tokyo Metropolitan Institute of Neuroscience</s1><s2>Tokyo 183-8526</s2><s3>JPN</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Miyamae, Takeaki" sort="Miyamae, Takeaki" uniqKey="Miyamae T" first="Takeaki" last="Miyamae">Takeaki Miyamae</name><affiliation><inist:fA14 i1="01"><s1>Department of Pharmacology, Yokohama City University School of Medicine</s1><s2>Yokohama 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type="abbreviated">Neurotoxicol. teratol.</title><idno type="ISSN">0892-0362</idno><imprint><date when="2002">2002</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neurotoxicology and teratology</title><title level="j" type="abbreviated">Neurotoxicol. teratol.</title><idno type="ISSN">0892-0362</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Chemotherapy</term><term>Clinical stage</term><term>Corpus striatum</term><term>In vitro</term><term>In vivo</term><term>Levodopa</term><term>Mechanism of action</term><term>Parkinson disease</term><term>Progressive</term><term>Rat</term><term>Toxicity</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Lévodopa</term><term>In vitro</term><term>In vivo</term><term>Rat</term><term>Animal</term><term>Traitement</term><term>Parkinson maladie</term><term>Chimiothérapie</term><term>Toxicité</term><term>Corps strié</term><term>Mécanisme action</term><term>Stade clinique</term><term>Progressif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">DOPA seems to be a neuromodulator in striata and hippocampal CAI and a neurotransmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS) and baroreflex pathways in the caudal ventrolateral medulla and rostral ventrolateral medulla in the brainstem of rats. DOPA recognition sites differ from dopamine (DA) D<sub>1</sub> and D<sub>2</sub> and ionotropic glutamate receptors. Via DOPA sites, DOPA stereoselectively releases by itself neuronal glutamate from in vitro and in vivo striata. In the cultured neurons, DOPA and DA cause neuron death via autoxidation. In addition, DOPA causes autoxidation-irrelevant neuron death via glutamate release. Furthermore, DOPA released by four-vessel occlusion seems to be an upstream causal factor for glutamate release and resultant delayed neuron death by brain ischemia in striata and hippocampal CA1. Glutamate has been regarded as a neurotransmitter of baroreflex pathways. Herein, we propose a new pathway that DOPA is a neurotransmitter of the primary aortic depressor nerve and glutamate is that of secondary neurons in neuronal microcircuits of'depressor sites in the NTS. DOPA seems to release unmeasurable, but functioning, endogenous glutamate from the secondary neurons via DOPA sites. A common following pathway may be ionotropic glutamate receptors-nNOS activation-NO production-baroreflex neurotransmission and delayed neuron death. However, we are concerned that DOPA therapy may accelerate neuronal degeneration process especially at progressive stages of Parkinson's disease.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0892-0362</s0></fA01><fA02 i1="01"><s0>NETEEC</s0></fA02><fA03 i2="1"><s0>Neurotoxicol. teratol.</s0></fA03><fA05><s2>24</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>DOPA causes glutamate release and delayed neuron death by brain ischemia in rats</s1></fA08><fA09 i1="01" i2="1" l="ENG"><s1>Milestones in Research on Neurotoxins and Neuroprotection: A Tribute to Professor Toshiharu Nagatsu</s1></fA09><fA11 i1="01" i2="1"><s1>MISU (Yoshimi)</s1></fA11><fA11 i1="02" i2="1"><s1>FURUKAWA (Nobuya)</s1></fA11><fA11 i1="03" i2="1"><s1>ARAI (Nobutaka)</s1></fA11><fA11 i1="04" i2="1"><s1>MIYAMAE (Takeaki)</s1></fA11><fA11 i1="05" i2="1"><s1>GOSHIMA (Yoshio)</s1></fA11><fA11 i1="06" i2="1"><s1>FUJITA (Kiyohide)</s1></fA11><fA12 i1="01" i2="1"><s1>NAOI (Makoto)</s1><s9>ed.</s9></fA12><fA12 i1="02" i2="1"><s1>PARVEZ (Hasan)</s1><s9>ed.</s9></fA12><fA12 i1="03" i2="1"><s1>MARUYAMA (Wakako)</s1><s9>ed.</s9></fA12><fA12 i1="04" i2="1"><s1>COLLINS (Michel A.)</s1><s9>ed.</s9></fA12><fA12 i1="05" i2="1"><s1>YOUDIM (Moussa B. H.)</s1><s9>ed.</s9></fA12><fA14 i1="01"><s1>Department of Pharmacology, Yokohama City University School of Medicine</s1><s2>Yokohama 236-0004</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Shinobu Hospital</s1><s2>Fukushima 960-1101</s2><s3>JPN</s3><sZ>1 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Oral and Maxillofacial Surgery, Yokohama City University School of Medicine</s1><s2>Yokohama 236-0004</s2><s3>JPN</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Clinical Neuropathology, Tokyo Metropolitan Institute of Neuroscience</s1><s2>Tokyo 183-8526</s2><s3>JPN</s3><sZ>3 aut.</sZ></fA14><fA15 i1="01"><s1>Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park</s1><s2>Mitake, Gifu 505-0116</s2><s3>JPN</s3><sZ>1 aut.</sZ></fA15><fA15 i1="02"><s1>Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS</s1><s2>91190 Gif sur Yvette</s2><s3>FRA</s3><sZ>2 aut.</sZ></fA15><fA15 i1="03"><s1>Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences</s1><s2>Obu, Aichi 474-8622</s2><s3>JPN</s3><sZ>3 aut.</sZ></fA15><fA15 i1="04"><s1>Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine</s1><s2>Maywood, IL 60153</s2><s3>USA</s3><sZ>4 aut.</sZ></fA15><fA15 i1="05"><s1>Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion</s1><s2>Haifa 31096</s2><s3>ISR</s3><sZ>5 aut.</sZ></fA15><fA20><s1>629-638</s1></fA20><fA21><s1>2002</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>18910</s2><s5>354000109244300080</s5></fA43><fA44><s0>0000</s0><s1>© 2003 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>60 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>03-0018077</s0></fA47><fA60><s1>P</s1><s2>C</s2></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neurotoxicology and teratology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>DOPA seems to be a neuromodulator in striata and hippocampal CAI and a neurotransmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS) and baroreflex pathways in the caudal ventrolateral medulla and rostral ventrolateral medulla in the brainstem of rats. DOPA recognition sites differ from dopamine (DA) D<sub>1</sub> and D<sub>2</sub> and ionotropic glutamate receptors. Via DOPA sites, DOPA stereoselectively releases by itself neuronal glutamate from in vitro and in vivo striata. In the cultured neurons, DOPA and DA cause neuron death via autoxidation. In addition, DOPA causes autoxidation-irrelevant neuron death via glutamate release. Furthermore, DOPA released by four-vessel occlusion seems to be an upstream causal factor for glutamate release and resultant delayed neuron death by brain ischemia in striata and hippocampal CA1. Glutamate has been regarded as a neurotransmitter of baroreflex pathways. Herein, we propose a new pathway that DOPA is a neurotransmitter of the primary aortic depressor nerve and glutamate is that of secondary neurons in neuronal microcircuits of'depressor sites in the NTS. DOPA seems to release unmeasurable, but functioning, endogenous glutamate from the secondary neurons via DOPA sites. A common following pathway may be ionotropic glutamate receptors-nNOS activation-NO production-baroreflex neurotransmission and delayed neuron death. However, we are concerned that DOPA therapy may accelerate neuronal degeneration process especially at progressive stages of Parkinson's disease.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B02B06</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Lévodopa</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Levodopa</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Levodopa</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>In vitro</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>In vitro</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>In vitro</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>In vivo</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>In vivo</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>In vivo</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Rat</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Rat</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Rata</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Animal</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Animal</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Animal</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Traitement</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Treatment</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Tratamiento</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>13</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Chimiothérapie</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Chemotherapy</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Quimioterapia</s0><s5>14</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Toxicité</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Toxicity</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Toxicidad</s0><s5>15</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Corps strié</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Corpus striatum</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Cuerpo estriado</s0><s5>16</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Mécanisme action</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Mechanism of action</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Mecanismo acción</s0><s5>17</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Stade clinique</s0><s5>19</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Clinical stage</s0><s5>19</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Estadio clínico</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Progressif</s0><s5>20</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Progressive</s0><s5>20</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Progresivo</s0><s5>20</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>69</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>69</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>69</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>70</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>70</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>70</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>71</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>71</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>71</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>72</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>72</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>72</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>73</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>73</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>73</s5></fC07><fN21><s1>006</s1></fN21><fN82><s1>PSI</s1></fN82></pA><pR><fA30 i1="01" i2="1" l="ENG"><s1>International Catecholamine Symposium</s1><s2>9</s2><s3>Kyoto JPN</s3><s4>2001-03-31</s4></fA30><fA30 i1="02" i2="1" l="ENG"><s1>International Joint Congresses on Progress in Alzheimer's and Parkinson's Disease</s1><s2>5</s2><s3>Kyoto JPN</s3><s4>2001-03-31</s4></fA30></pR></standard><server><NO>PASCAL 03-0018077 INIST</NO><ET>DOPA causes glutamate release and delayed neuron death by brain ischemia in rats</ET><AU>MISU (Yoshimi); FURUKAWA (Nobuya); ARAI (Nobutaka); MIYAMAE (Takeaki); GOSHIMA (Yoshio); FUJITA (Kiyohide); NAOI (Makoto); PARVEZ (Hasan); MARUYAMA (Wakako); COLLINS (Michel A.); YOUDIM (Moussa B. H.)</AU><AF>Department of Pharmacology, Yokohama City University School of Medicine/Yokohama 236-0004/Japon (1 aut., 2 aut., 4 aut., 5 aut.); Shinobu Hospital/Fukushima 960-1101/Japon (1 aut.); Department of Oral and Maxillofacial Surgery, Yokohama City University School of Medicine/Yokohama 236-0004/Japon (2 aut., 6 aut.); Department of Clinical Neuropathology, Tokyo Metropolitan Institute of Neuroscience/Tokyo 183-8526/Japon (3 aut.); Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park/Mitake, Gifu 505-0116/Japon (1 aut.); Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut.); Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences/Obu, Aichi 474-8622/Japon (3 aut.); Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine/Maywood, IL 60153/Etats-Unis (4 aut.); Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion/Haifa 31096/Israël (5 aut.)</AF><DT>Publication en série; Congrès; Niveau analytique</DT><SO>Neurotoxicology and teratology; ISSN 0892-0362; Coden NETEEC; Etats-Unis; Da. 2002; Vol. 24; No. 5; Pp. 629-638; Bibl. 60 ref.</SO><LA>Anglais</LA><EA>DOPA seems to be a neuromodulator in striata and hippocampal CAI and a neurotransmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS) and baroreflex pathways in the caudal ventrolateral medulla and rostral ventrolateral medulla in the brainstem of rats. DOPA recognition sites differ from dopamine (DA) D<sub>1</sub> and D<sub>2</sub> and ionotropic glutamate receptors. Via DOPA sites, DOPA stereoselectively releases by itself neuronal glutamate from in vitro and in vivo striata. In the cultured neurons, DOPA and DA cause neuron death via autoxidation. In addition, DOPA causes autoxidation-irrelevant neuron death via glutamate release. Furthermore, DOPA released by four-vessel occlusion seems to be an upstream causal factor for glutamate release and resultant delayed neuron death by brain ischemia in striata and hippocampal CA1. Glutamate has been regarded as a neurotransmitter of baroreflex pathways. Herein, we propose a new pathway that DOPA is a neurotransmitter of the primary aortic depressor nerve and glutamate is that of secondary neurons in neuronal microcircuits of'depressor sites in the NTS. DOPA seems to release unmeasurable, but functioning, endogenous glutamate from the secondary neurons via DOPA sites. A common following pathway may be ionotropic glutamate receptors-nNOS activation-NO production-baroreflex neurotransmission and delayed neuron death. However, we are concerned that DOPA therapy may accelerate neuronal degeneration process especially at progressive stages of Parkinson's disease.</EA><CC>002B17G; 002B02B06</CC><FD>Lévodopa; In vitro; In vivo; Rat; Animal; Traitement; Parkinson maladie; Chimiothérapie; Toxicité; Corps strié; Mécanisme action; Stade clinique; Progressif</FD><FG>Rodentia; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG><ED>Levodopa; In vitro; In vivo; Rat; Animal; Treatment; Parkinson disease; Chemotherapy; Toxicity; Corpus striatum; Mechanism of action; Clinical stage; Progressive</ED><EG>Rodentia; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG><SD>Levodopa; In vitro; In vivo; Rata; Animal; Tratamiento; Parkinson enfermedad; Quimioterapia; Toxicidad; Cuerpo estriado; Mecanismo acción; Estadio clínico; Progresivo</SD><LO>INIST-18910.354000109244300080</LO><ID>03-0018077</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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