A stereological study on the neuroprotective actions of acute Modafinil treatment on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigral lesions of the male black mouse
Identifieur interne : 001441 ( PascalFrancis/Corpus ); précédent : 001440; suivant : 001442A stereological study on the neuroprotective actions of acute Modafinil treatment on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigral lesions of the male black mouse
Auteurs : J. A. Aguirre ; A. Cintra ; J. Hillion ; J. A. Narvaez ; A. Jansson ; T. Antonelli ; L. Ferraro ; F. A. Rambert ; K. FuxeSource :
- Neuroscience letters [ 0304-3940 ] ; 1999.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
The effect of an acute administration of the vigilance-promoting drug modafinil ((±)(diphenyl-methyl)-sulfinyl-2 acetamide ; Modiodal) on the nigrostriatal dopamine system was studied after damage induced by MPTP (1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine) by means of immunohistochemistry for tyrosine hydroxylase (TH) and a stereological method. MPTP (40 mg/kg) reduced from 24 380 ± 902 to 13 501 ± 522 and from 37 868 ± 3300 to 20 568 ± 1270, respectively, the number of TH immunoreactive (IR) and non-TH IR nigral neurons. Co-administration of Modafinil restored to normal the number of these neuronal populations. MPTP treatment induced also a reduction in the volume of TH IR neurons, which was counteracted by Modafinil administration. The data provide morphological evidence, based on unbiased stereological analysis, for a potential neuroprotective role of Modafinil, not only in dopaminergic neurons, but also with a similar magnitude in the non-DA nerve cell population of the substantia nigra after MPTP lesion. These results suggest that Modafinil has a neuroprotective role in the substantia nigra via a still undefined mechanism in which a crucial role of DA uptake blockade should be excluded. Modafinil may therefore have a therapeutic potential in neurodegenerative processes such as those occurring in Parkinson's disease.
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NO : | PASCAL 99-0547776 INIST |
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ET : | A stereological study on the neuroprotective actions of acute Modafinil treatment on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigral lesions of the male black mouse |
AU : | AGUIRRE (J. A.); CINTRA (A.); HILLION (J.); NARVAEZ (J. A.); JANSSON (A.); ANTONELLI (T.); FERRARO (L.); RAMBERT (F. A.); FUXE (K.) |
AF : | Department of Physiology, School of Medicine/29080, Malaga/Espagne (1 aut., 4 aut.); Department of Neuroscience, Karolinska Institutet/17177, Solna/Suède (2 aut., 3 aut., 5 aut., 9 aut.); Department of Experimental and Clinical Medicine, Section of Pharmacology, University of Ferrara/Ferrara/Italie (6 aut., 7 aut.); Laboratoire L. Lafon/Maisons-Alfort/France (8 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neuroscience letters; ISSN 0304-3940; Coden NELED5; Irlande; Da. 1999; Vol. 275; No. 3; Pp. 215-218; Bibl. 17 ref. |
LA : | Anglais |
EA : | The effect of an acute administration of the vigilance-promoting drug modafinil ((±)(diphenyl-methyl)-sulfinyl-2 acetamide ; Modiodal) on the nigrostriatal dopamine system was studied after damage induced by MPTP (1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine) by means of immunohistochemistry for tyrosine hydroxylase (TH) and a stereological method. MPTP (40 mg/kg) reduced from 24 380 ± 902 to 13 501 ± 522 and from 37 868 ± 3300 to 20 568 ± 1270, respectively, the number of TH immunoreactive (IR) and non-TH IR nigral neurons. Co-administration of Modafinil restored to normal the number of these neuronal populations. MPTP treatment induced also a reduction in the volume of TH IR neurons, which was counteracted by Modafinil administration. The data provide morphological evidence, based on unbiased stereological analysis, for a potential neuroprotective role of Modafinil, not only in dopaminergic neurons, but also with a similar magnitude in the non-DA nerve cell population of the substantia nigra after MPTP lesion. These results suggest that Modafinil has a neuroprotective role in the substantia nigra via a still undefined mechanism in which a crucial role of DA uptake blockade should be excluded. Modafinil may therefore have a therapeutic potential in neurodegenerative processes such as those occurring in Parkinson's disease. |
CC : | 002B02B10 |
FD : | Lésion; Locus niger; Modafinil; Neuroprotecteur; Stéréologie; Dopamine; Parkinson maladie; Modèle animal; Mâle; MPTP |
FG : | Encéphale; Système nerveux central; Neurotransmetteur; Catécholamine; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative |
ED : | Lesion; Locus niger; Modafinil; Neuroprotective agent; Stereology; Dopamine; Parkinson disease; Animal model; Male |
EG : | Brain (vertebrata); Central nervous system; Neurotransmitter; Catecholamine; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease |
SD : | Lesión; Locus níger; Modafinilo; Neuroprotector; Estereología; Dopamina; Parkinson enfermedad; Modelo animal; Macho |
LO : | INIST-17240.354000080503700160 |
ID : | 99-0547776 |
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Pascal:99-0547776Le document en format XML
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<front><div type="abstract" xml:lang="en">The effect of an acute administration of the vigilance-promoting drug modafinil ((±)(diphenyl-methyl)-sulfinyl-2 acetamide ; Modiodal) on the nigrostriatal dopamine system was studied after damage induced by MPTP (1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine) by means of immunohistochemistry for tyrosine hydroxylase (TH) and a stereological method. MPTP (40 mg/kg) reduced from 24 380 ± 902 to 13 501 ± 522 and from 37 868 ± 3300 to 20 568 ± 1270, respectively, the number of TH immunoreactive (IR) and non-TH IR nigral neurons. Co-administration of Modafinil restored to normal the number of these neuronal populations. MPTP treatment induced also a reduction in the volume of TH IR neurons, which was counteracted by Modafinil administration. The data provide morphological evidence, based on unbiased stereological analysis, for a potential neuroprotective role of Modafinil, not only in dopaminergic neurons, but also with a similar magnitude in the non-DA nerve cell population of the substantia nigra after MPTP lesion. These results suggest that Modafinil has a neuroprotective role in the substantia nigra via a still undefined mechanism in which a crucial role of DA uptake blockade should be excluded. Modafinil may therefore have a therapeutic potential in neurodegenerative processes such as those occurring in Parkinson's disease.</div>
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<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Modèle animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Animal model</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Modelo animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Mâle</s0>
<s5>54</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Male</s0>
<s5>54</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Macho</s0>
<s5>54</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>MPTP</s0>
<s4>INC</s4>
<s5>78</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>23</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Brain (vertebrata)</s0>
<s5>23</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>23</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>24</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>24</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>24</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>35</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>35</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>35</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>36</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>36</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>36</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso patología</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>Encéphale pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Encéfalo 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>
<fC07 i1="09" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fN21><s1>355</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 99-0547776 INIST</NO>
<ET>A stereological study on the neuroprotective actions of acute Modafinil treatment on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced nigral lesions of the male black mouse</ET>
<AU>AGUIRRE (J. A.); CINTRA (A.); HILLION (J.); NARVAEZ (J. A.); JANSSON (A.); ANTONELLI (T.); FERRARO (L.); RAMBERT (F. A.); FUXE (K.)</AU>
<AF>Department of Physiology, School of Medicine/29080, Malaga/Espagne (1 aut., 4 aut.); Department of Neuroscience, Karolinska Institutet/17177, Solna/Suède (2 aut., 3 aut., 5 aut., 9 aut.); Department of Experimental and Clinical Medicine, Section of Pharmacology, University of Ferrara/Ferrara/Italie (6 aut., 7 aut.); Laboratoire L. Lafon/Maisons-Alfort/France (8 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuroscience letters; ISSN 0304-3940; Coden NELED5; Irlande; Da. 1999; Vol. 275; No. 3; Pp. 215-218; Bibl. 17 ref.</SO>
<LA>Anglais</LA>
<EA>The effect of an acute administration of the vigilance-promoting drug modafinil ((±)(diphenyl-methyl)-sulfinyl-2 acetamide ; Modiodal) on the nigrostriatal dopamine system was studied after damage induced by MPTP (1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine) by means of immunohistochemistry for tyrosine hydroxylase (TH) and a stereological method. MPTP (40 mg/kg) reduced from 24 380 ± 902 to 13 501 ± 522 and from 37 868 ± 3300 to 20 568 ± 1270, respectively, the number of TH immunoreactive (IR) and non-TH IR nigral neurons. Co-administration of Modafinil restored to normal the number of these neuronal populations. MPTP treatment induced also a reduction in the volume of TH IR neurons, which was counteracted by Modafinil administration. The data provide morphological evidence, based on unbiased stereological analysis, for a potential neuroprotective role of Modafinil, not only in dopaminergic neurons, but also with a similar magnitude in the non-DA nerve cell population of the substantia nigra after MPTP lesion. These results suggest that Modafinil has a neuroprotective role in the substantia nigra via a still undefined mechanism in which a crucial role of DA uptake blockade should be excluded. Modafinil may therefore have a therapeutic potential in neurodegenerative processes such as those occurring in Parkinson's disease.</EA>
<CC>002B02B10</CC>
<FD>Lésion; Locus niger; Modafinil; Neuroprotecteur; Stéréologie; Dopamine; Parkinson maladie; Modèle animal; Mâle; MPTP</FD>
<FG>Encéphale; Système nerveux central; Neurotransmetteur; Catécholamine; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG>
<ED>Lesion; Locus niger; Modafinil; Neuroprotective agent; Stereology; Dopamine; Parkinson disease; Animal model; Male</ED>
<EG>Brain (vertebrata); Central nervous system; Neurotransmitter; Catecholamine; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Lesión; Locus níger; Modafinilo; Neuroprotector; Estereología; Dopamina; Parkinson enfermedad; Modelo animal; Macho</SD>
<LO>INIST-17240.354000080503700160</LO>
<ID>99-0547776</ID>
</server>
</inist>
</record>
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