La maladie de Parkinson en France (serveur d'exploration)

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Ectopic expression of the TrkA receptor in adult dopaminergic mesencephalic neurons promotes retrograde axonal NGF transport and NGF-dependent neuroprotection

Identifieur interne : 000D89 ( PascalFrancis/Checkpoint ); précédent : 000D88; suivant : 000D90

Ectopic expression of the TrkA receptor in adult dopaminergic mesencephalic neurons promotes retrograde axonal NGF transport and NGF-dependent neuroprotection

Auteurs : Benoit Melchior [France] ; Véronique Nerriere-Daguin [France] ; David-A. Laplaud [France] ; Séverine Remy [France] ; Sandrine Wiertlewski [France] ; Isabelle Neveu [France] ; Philippe Naveilhan [France] ; Susan O. Meakin [Canada] ; Philippe Brachet [France]

Source :

RBID : Pascal:04-0162976

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Abstract

A recombinant adeno-associated virus (rAAV) was used to investigate the impact of an ectopic expression of the NGF high-affinity receptor in adult neurons. The rat TrkA cDNA cloned in a pCMX vector was first tagged with a human c-Myc sequence. The resulting vector was shown to encode a functional receptor which promoted the expression of TrkA immunoreactivity upon transfection of 293 fibroblasts or nnr5 cells, a TrkA-defective variant of PC 12 cells. These cells also accumulate TrkA transcripts upon transfection and extended neurites in the presence of NGF. Therefore, the TrkAmyc cassette was inserted into the pSSV9 plasmid. The new vectors shared properties similar to pCMX TrkAmyc in 293 and nnr5 cells and enabled the preparation of rAAV TrkAmyc viruses. Unilateral injection of this rAAV into the substantia nigra (SN) resulted in a protracted expression of TrkA (or c-Myc) immunoreactivity in numerous cell bodies, including tyrosine-hydroxylase (TH)-positive dopaminergic neurons. The presence of TrkA receptors in corresponding striatal dopaminergic endings was demonstrated by the advent of a striato-nigral retrograde axonal transport of 125I-NGF. Likewise, ectopic expression of TrkA in neurons of the parafascicular thalamic nucleus promoted a striatofuge transport of NGF toward this structure. To investigate whether ectopic expression of TrkA in SN neurons may confer neuroprotection, lesions were induced by 6-hydroxydopamine in striata located ipsilateral to the virus injection site. NGF or vehicle were next delivered dorsally to the virus-treated SN for 2 weeks, before sacrifice and processing of brains for TH-immunohistochemistry. NGF treatment, in contrast to treatment with vehicle, significantly enhanced the number of dopaminergic neurons counted in the lesioned SN. These data suggest that ectopic TrkA can mediate the trophic actions of NGF and influence neuronal plasticity in vivo.


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Pascal:04-0162976

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<div type="abstract" xml:lang="en">A recombinant adeno-associated virus (rAAV) was used to investigate the impact of an ectopic expression of the NGF high-affinity receptor in adult neurons. The rat TrkA cDNA cloned in a pCMX vector was first tagged with a human c-Myc sequence. The resulting vector was shown to encode a functional receptor which promoted the expression of TrkA immunoreactivity upon transfection of 293 fibroblasts or nnr5 cells, a TrkA-defective variant of PC 12 cells. These cells also accumulate TrkA transcripts upon transfection and extended neurites in the presence of NGF. Therefore, the TrkA
<sub>myc</sub>
cassette was inserted into the pSSV9 plasmid. The new vectors shared properties similar to pCMX TrkA
<sub>myc</sub>
in 293 and nnr5 cells and enabled the preparation of rAAV TrkA
<sub>myc</sub>
viruses. Unilateral injection of this rAAV into the substantia nigra (SN) resulted in a protracted expression of TrkA (or c-Myc) immunoreactivity in numerous cell bodies, including tyrosine-hydroxylase (TH)-positive dopaminergic neurons. The presence of TrkA receptors in corresponding striatal dopaminergic endings was demonstrated by the advent of a striato-nigral retrograde axonal transport of
<sup>125</sup>
I-NGF. Likewise, ectopic expression of TrkA in neurons of the parafascicular thalamic nucleus promoted a striatofuge transport of NGF toward this structure. To investigate whether ectopic expression of TrkA in SN neurons may confer neuroprotection, lesions were induced by 6-hydroxydopamine in striata located ipsilateral to the virus injection site. NGF or vehicle were next delivered dorsally to the virus-treated SN for 2 weeks, before sacrifice and processing of brains for TH-immunohistochemistry. NGF treatment, in contrast to treatment with vehicle, significantly enhanced the number of dopaminergic neurons counted in the lesioned SN. These data suggest that ectopic TrkA can mediate the trophic actions of NGF and influence neuronal plasticity in vivo.</div>
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<s1>MELCHIOR (Benoit)</s1>
</fA11>
<fA11 i1="02" i2="1">
<s1>NERRIERE-DAGUIN (Véronique)</s1>
</fA11>
<fA11 i1="03" i2="1">
<s1>LAPLAUD (David-A.)</s1>
</fA11>
<fA11 i1="04" i2="1">
<s1>REMY (Séverine)</s1>
</fA11>
<fA11 i1="05" i2="1">
<s1>WIERTLEWSKI (Sandrine)</s1>
</fA11>
<fA11 i1="06" i2="1">
<s1>NEVEU (Isabelle)</s1>
</fA11>
<fA11 i1="07" i2="1">
<s1>NAVEILHAN (Philippe)</s1>
</fA11>
<fA11 i1="08" i2="1">
<s1>MEAKIN (Susan O.)</s1>
</fA11>
<fA11 i1="09" i2="1">
<s1>BRACHET (Philippe)</s1>
</fA11>
<fA14 i1="01">
<s1>Institut National de la Samé et de la Recherche Médicale, Unité 437</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Clinique Neurologique, Centre Hospitalier Universitaire</s1>
<s2>44093 Nantes</s2>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>The Robarts Research Institute</s1>
<s2>London, Ontario</s2>
<s3>CAN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA20>
<s1>367-378</s1>
</fA20>
<fA21>
<s1>2003</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>9181</s2>
<s5>354000113272860100</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2004 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>2 p.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>04-0162976</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Experimental neurology : (Print)</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>A recombinant adeno-associated virus (rAAV) was used to investigate the impact of an ectopic expression of the NGF high-affinity receptor in adult neurons. The rat TrkA cDNA cloned in a pCMX vector was first tagged with a human c-Myc sequence. The resulting vector was shown to encode a functional receptor which promoted the expression of TrkA immunoreactivity upon transfection of 293 fibroblasts or nnr5 cells, a TrkA-defective variant of PC 12 cells. These cells also accumulate TrkA transcripts upon transfection and extended neurites in the presence of NGF. Therefore, the TrkA
<sub>myc</sub>
cassette was inserted into the pSSV9 plasmid. The new vectors shared properties similar to pCMX TrkA
<sub>myc</sub>
in 293 and nnr5 cells and enabled the preparation of rAAV TrkA
<sub>myc</sub>
viruses. Unilateral injection of this rAAV into the substantia nigra (SN) resulted in a protracted expression of TrkA (or c-Myc) immunoreactivity in numerous cell bodies, including tyrosine-hydroxylase (TH)-positive dopaminergic neurons. The presence of TrkA receptors in corresponding striatal dopaminergic endings was demonstrated by the advent of a striato-nigral retrograde axonal transport of
<sup>125</sup>
I-NGF. Likewise, ectopic expression of TrkA in neurons of the parafascicular thalamic nucleus promoted a striatofuge transport of NGF toward this structure. To investigate whether ectopic expression of TrkA in SN neurons may confer neuroprotection, lesions were induced by 6-hydroxydopamine in striata located ipsilateral to the virus injection site. NGF or vehicle were next delivered dorsally to the virus-treated SN for 2 weeks, before sacrifice and processing of brains for TH-immunohistochemistry. NGF treatment, in contrast to treatment with vehicle, significantly enhanced the number of dopaminergic neurons counted in the lesioned SN. These data suggest that ectopic TrkA can mediate the trophic actions of NGF and influence neuronal plasticity in vivo.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Fibroblaste</s0>
<s5>02</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Fibroblast</s0>
<s5>02</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Fibroblasto</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Tyrosine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Tyrosine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Tirosina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Démence Alzheimer</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Alzheimer disease</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Demencia Alzheimer</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Immunohistochimie</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Immunohistochemistry</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Inmunohistoquímica</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Thérapie génique</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Gene therapy</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Terapia génica</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>DNA complémentaire</s0>
<s5>16</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Complementary DNA</s0>
<s5>16</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>DNA complementario</s0>
<s5>16</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Neurone dopaminergique</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Dopaminergic neuron</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Neurona dopaminérgica</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Facteur croissance nerf</s0>
<s5>18</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Nerve growth factor</s0>
<s5>18</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Factor crecimiento nervio</s0>
<s5>18</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Virus recombinant</s0>
<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Recombinant virus</s0>
<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Virus recombinante</s0>
<s5>20</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG">
<s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA">
<s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE">
<s0>Rat</s0>
<s5>22</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Rat</s0>
<s5>22</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Rata</s0>
<s5>22</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Gène onc cellulaire</s0>
<s5>24</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>C-Onc gene</s0>
<s5>24</s5>
<s6>«C»-Onc gene</s6>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Gen onc celular</s0>
<s5>24</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE">
<s0>Aminoacide</s0>
<s5>25</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Aminoacid</s0>
<s5>25</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Aminoácido</s0>
<s5>25</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE">
<s0>Transfection</s0>
<s5>35</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG">
<s0>Transfection</s0>
<s5>35</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA">
<s0>Transfección</s0>
<s5>35</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>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fN21>
<s1>103</s1>
</fN21>
<fN82>
<s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations>
<list>
<country>
<li>Canada</li>
<li>France</li>
</country>
<region>
<li>Pays de la Loire</li>
</region>
<settlement>
<li>Nantes</li>
</settlement>
</list>
<tree>
<country name="France">
<region name="Pays de la Loire">
<name sortKey="Melchior, Benoit" sort="Melchior, Benoit" uniqKey="Melchior B" first="Benoit" last="Melchior">Benoit Melchior</name>
</region>
<name sortKey="Brachet, Philippe" sort="Brachet, Philippe" uniqKey="Brachet P" first="Philippe" last="Brachet">Philippe Brachet</name>
<name sortKey="Laplaud, David A" sort="Laplaud, David A" uniqKey="Laplaud D" first="David-A." last="Laplaud">David-A. Laplaud</name>
<name sortKey="Laplaud, David A" sort="Laplaud, David A" uniqKey="Laplaud D" first="David-A." last="Laplaud">David-A. Laplaud</name>
<name sortKey="Naveilhan, Philippe" sort="Naveilhan, Philippe" uniqKey="Naveilhan P" first="Philippe" last="Naveilhan">Philippe Naveilhan</name>
<name sortKey="Nerriere Daguin, Veronique" sort="Nerriere Daguin, Veronique" uniqKey="Nerriere Daguin V" first="Véronique" last="Nerriere-Daguin">Véronique Nerriere-Daguin</name>
<name sortKey="Neveu, Isabelle" sort="Neveu, Isabelle" uniqKey="Neveu I" first="Isabelle" last="Neveu">Isabelle Neveu</name>
<name sortKey="Remy, Severine" sort="Remy, Severine" uniqKey="Remy S" first="Séverine" last="Remy">Séverine Remy</name>
<name sortKey="Wiertlewski, Sandrine" sort="Wiertlewski, Sandrine" uniqKey="Wiertlewski S" first="Sandrine" last="Wiertlewski">Sandrine Wiertlewski</name>
</country>
<country name="Canada">
<noRegion>
<name sortKey="Meakin, Susan O" sort="Meakin, Susan O" uniqKey="Meakin S" first="Susan O." last="Meakin">Susan O. Meakin</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

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   |texte=   Ectopic expression of the TrkA receptor in adult dopaminergic mesencephalic neurons promotes retrograde axonal NGF transport and NGF-dependent neuroprotection
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