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

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The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurons in Parkinson's disease

Identifieur interne : 001480 ( PascalFrancis/Corpus ); précédent : 001479; suivant : 001481

The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurons in Parkinson's disease

Auteurs : P. Damier ; E. C. Hirsch ; Y. Agid ; A. M. Graybiel

Source :

RBID : Pascal:99-0412231

Descripteurs français

English descriptors

Abstract

To achieve accuracy in studying the patterns of loss of midbrain dopamine-containing neurons in Parkinson's disease, we used compartmental patterns of calbindin D28K immunostaining to subdivide the substantia nigra with landmarks independent of the degenerative process. Within the substantia nigra pars compacta, we identified dopamine-containing neurons in the calbindin-rich regions ('matrix') and in five calbindin-poor pockets ('nigrosomes') defined by analysis of the three-dimensional networks formed by the calbindin-poor zones. These zones were recognizable in all of the brains, despite severe loss of dopamine-containing neurons. The degree of loss of dopamine-containing neurons in the substantia nigra pars compacta was related to the duration of the disease, and the cell loss followed a strict order. The degree of neuronal loss was significantly higher in the nigrosomes than in the matrix. Depletion was maximum (98%) in the main pocket (nigrosome 1), located in the caudal and mediolateral part of the substantia nigra pars compacta. Progressively less cell loss was detectable in more medial and more rostral nigrosomes, following the stereotyped order of nigrosome 1 > nigrosome 2 > nigrosome 4 > nigrosome 3 > nigrosome 5. A parallel, but lesser, caudorostral gradient of cell loss was observed for dopamine-containing neurons included in the matrix. This pattern of neuronal loss was consistent from one parkinsonian substantia nigra pars compacta to another. The spatiotemporal progression of neuronal loss related to disease duration can thus be drawn in the substantia nigra pars compacta for each Parkinson's disease patient: depletion begins in the main pocket (nigrosome 1) and then spreads to other nigrosomes and the matrix along rostral, medial and dorsal axes of progression.

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C01 01    ENG  @0 To achieve accuracy in studying the patterns of loss of midbrain dopamine-containing neurons in Parkinson's disease, we used compartmental patterns of calbindin D28K immunostaining to subdivide the substantia nigra with landmarks independent of the degenerative process. Within the substantia nigra pars compacta, we identified dopamine-containing neurons in the calbindin-rich regions ('matrix') and in five calbindin-poor pockets ('nigrosomes') defined by analysis of the three-dimensional networks formed by the calbindin-poor zones. These zones were recognizable in all of the brains, despite severe loss of dopamine-containing neurons. The degree of loss of dopamine-containing neurons in the substantia nigra pars compacta was related to the duration of the disease, and the cell loss followed a strict order. The degree of neuronal loss was significantly higher in the nigrosomes than in the matrix. Depletion was maximum (98%) in the main pocket (nigrosome 1), located in the caudal and mediolateral part of the substantia nigra pars compacta. Progressively less cell loss was detectable in more medial and more rostral nigrosomes, following the stereotyped order of nigrosome 1 > nigrosome 2 > nigrosome 4 > nigrosome 3 > nigrosome 5. A parallel, but lesser, caudorostral gradient of cell loss was observed for dopamine-containing neurons included in the matrix. This pattern of neuronal loss was consistent from one parkinsonian substantia nigra pars compacta to another. The spatiotemporal progression of neuronal loss related to disease duration can thus be drawn in the substantia nigra pars compacta for each Parkinson's disease patient: depletion begins in the main pocket (nigrosome 1) and then spreads to other nigrosomes and the matrix along rostral, medial and dorsal axes of progression.
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Format Inist (serveur)

NO : PASCAL 99-0412231 INIST
ET : The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurons in Parkinson's disease
AU : DAMIER (P.); HIRSCH (E. C.); AGID (Y.); GRAYBIEL (A. M.)
AF : INSERM U289, Hôpital de la Salpêtrière/Paris/France (1 aut., 2 aut., 3 aut.); Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology/Cambridge, Massachusetts/Etats-Unis (1 aut., 4 aut.)
DT : Publication en série; Niveau analytique
SO : Brain; ISSN 0006-8950; Royaume-Uni; Da. 1999; Vol. 122; No. p.8; Pp. 1437-1448; Bibl. 15 ref.
LA : Anglais
EA : To achieve accuracy in studying the patterns of loss of midbrain dopamine-containing neurons in Parkinson's disease, we used compartmental patterns of calbindin D28K immunostaining to subdivide the substantia nigra with landmarks independent of the degenerative process. Within the substantia nigra pars compacta, we identified dopamine-containing neurons in the calbindin-rich regions ('matrix') and in five calbindin-poor pockets ('nigrosomes') defined by analysis of the three-dimensional networks formed by the calbindin-poor zones. These zones were recognizable in all of the brains, despite severe loss of dopamine-containing neurons. The degree of loss of dopamine-containing neurons in the substantia nigra pars compacta was related to the duration of the disease, and the cell loss followed a strict order. The degree of neuronal loss was significantly higher in the nigrosomes than in the matrix. Depletion was maximum (98%) in the main pocket (nigrosome 1), located in the caudal and mediolateral part of the substantia nigra pars compacta. Progressively less cell loss was detectable in more medial and more rostral nigrosomes, following the stereotyped order of nigrosome 1 > nigrosome 2 > nigrosome 4 > nigrosome 3 > nigrosome 5. A parallel, but lesser, caudorostral gradient of cell loss was observed for dopamine-containing neurons included in the matrix. This pattern of neuronal loss was consistent from one parkinsonian substantia nigra pars compacta to another. The spatiotemporal progression of neuronal loss related to disease duration can thus be drawn in the substantia nigra pars compacta for each Parkinson's disease patient: depletion begins in the main pocket (nigrosome 1) and then spreads to other nigrosomes and the matrix along rostral, medial and dorsal axes of progression.
CC : 002B17G
FD : Parkinson maladie; Neurone dopaminergique; Dopamine; Locus niger; Cholécalcine; Distribution; Immunohistochimie; Anatomopathologie; Exploration; Homme
FG : Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative
ED : Parkinson disease; Dopaminergic neuron; Dopamine; Locus niger; Calbindin; Distribution; Immunohistochemistry; Pathology; Exploration; Human
EG : Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease
SD : Parkinson enfermedad; Neurona dopaminérgica; Dopamina; Locus níger; Coleocalcina; Distribución; Inmunohistoquímica; Anatomía patológica; Exploración; Hombre
LO : INIST-998.354000089290940040
ID : 99-0412231

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Pascal:99-0412231

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<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Locus niger</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Locus niger</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Locus níger</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Cholécalcine</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Calbindin</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Coleocalcina</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Distribution</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Distribution</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Distribución</s0>
<s5>10</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Immunohistochimie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Immunohistochemistry</s0>
<s5>17</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Inmunohistoquímica</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Anatomopathologie</s0>
<s5>18</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Pathology</s0>
<s5>18</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Anatomía patológica</s0>
<s5>18</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Exploration</s0>
<s5>19</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Exploration</s0>
<s5>19</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Exploración</s0>
<s5>19</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fN21>
<s1>263</s1>
</fN21>
</pA>
</standard>
<server>
<NO>PASCAL 99-0412231 INIST</NO>
<ET>The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurons in Parkinson's disease</ET>
<AU>DAMIER (P.); HIRSCH (E. C.); AGID (Y.); GRAYBIEL (A. M.)</AU>
<AF>INSERM U289, Hôpital de la Salpêtrière/Paris/France (1 aut., 2 aut., 3 aut.); Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology/Cambridge, Massachusetts/Etats-Unis (1 aut., 4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 1999; Vol. 122; No. p.8; Pp. 1437-1448; Bibl. 15 ref.</SO>
<LA>Anglais</LA>
<EA>To achieve accuracy in studying the patterns of loss of midbrain dopamine-containing neurons in Parkinson's disease, we used compartmental patterns of calbindin D
<sub>28K</sub>
immunostaining to subdivide the substantia nigra with landmarks independent of the degenerative process. Within the substantia nigra pars compacta, we identified dopamine-containing neurons in the calbindin-rich regions ('matrix') and in five calbindin-poor pockets ('nigrosomes') defined by analysis of the three-dimensional networks formed by the calbindin-poor zones. These zones were recognizable in all of the brains, despite severe loss of dopamine-containing neurons. The degree of loss of dopamine-containing neurons in the substantia nigra pars compacta was related to the duration of the disease, and the cell loss followed a strict order. The degree of neuronal loss was significantly higher in the nigrosomes than in the matrix. Depletion was maximum (98%) in the main pocket (nigrosome 1), located in the caudal and mediolateral part of the substantia nigra pars compacta. Progressively less cell loss was detectable in more medial and more rostral nigrosomes, following the stereotyped order of nigrosome 1 > nigrosome 2 > nigrosome 4 > nigrosome 3 > nigrosome 5. A parallel, but lesser, caudorostral gradient of cell loss was observed for dopamine-containing neurons included in the matrix. This pattern of neuronal loss was consistent from one parkinsonian substantia nigra pars compacta to another. The spatiotemporal progression of neuronal loss related to disease duration can thus be drawn in the substantia nigra pars compacta for each Parkinson's disease patient: depletion begins in the main pocket (nigrosome 1) and then spreads to other nigrosomes and the matrix along rostral, medial and dorsal axes of progression.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Neurone dopaminergique; Dopamine; Locus niger; Cholécalcine; Distribution; Immunohistochimie; Anatomopathologie; Exploration; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG>
<ED>Parkinson disease; Dopaminergic neuron; Dopamine; Locus niger; Calbindin; Distribution; Immunohistochemistry; Pathology; Exploration; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Parkinson enfermedad; Neurona dopaminérgica; Dopamina; Locus níger; Coleocalcina; Distribución; Inmunohistoquímica; Anatomía patológica; Exploración; Hombre</SD>
<LO>INIST-998.354000089290940040</LO>
<ID>99-0412231</ID>
</server>
</inist>
</record>

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