Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction
Identifieur interne : 002A68 ( Main/Curation ); précédent : 002A67; suivant : 002A69Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction
Auteurs : Ichiro Kanazawa ; Shin Kwak ; Hidenao Sasaki ; Osamu Muramoto ; Toshio Mizutani ; Akira Hori ; Nobuyuki NukinaSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1987.
Abstract
γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.
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DOI: 10.1016/0022-510X(88)90020-2
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Ichiro Kanazawa<affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation><affiliation><mods:affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 113 Japan</wicri:noCountry></affiliation><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation><affiliation><mods:affiliation>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 118 Japan</wicri:noCountry></affiliation><affiliation><mods:affiliation>Department of Pathology, University of Göttingen, Göttingen F.R.G.</mods:affiliation><wicri:noCountry code="subField">Göttingen F.R.G.</wicri:noCountry></affiliation><affiliation><mods:affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 113 Japan</wicri:noCountry></affiliation>Le document en format XML
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uniqKey="Sasaki H" first="Hidenao" last="Sasaki">Hidenao Sasaki</name><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Muramoto, Osamu" sort="Muramoto, Osamu" uniqKey="Muramoto O" first="Osamu" last="Muramoto">Osamu Muramoto</name><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Mizutani, Toshio" sort="Mizutani, Toshio" uniqKey="Mizutani T" first="Toshio" last="Mizutani">Toshio Mizutani</name><affiliation><mods:affiliation>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 118 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Hori, Akira" sort="Hori, Akira" uniqKey="Hori A" first="Akira" last="Hori">Akira Hori</name><affiliation><mods:affiliation>Department of Pathology, University of Göttingen, Göttingen F.R.G.</mods:affiliation><wicri:noCountry code="subField">Göttingen F.R.G.</wicri:noCountry></affiliation></author><author><name sortKey="Nukina, Nobuyuki" sort="Nukina, Nobuyuki" uniqKey="Nukina N" first="Nobuyuki" last="Nukina">Nobuyuki Nukina</name><affiliation><mods:affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 113 Japan</wicri:noCountry></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:60F8C350DF5B61978A2C138D6BBF993EF15F084C</idno><date when="1988" year="1988">1988</date><idno type="doi">10.1016/0022-510X(88)90020-2</idno><idno type="url">https://api.istex.fr/document/60F8C350DF5B61978A2C138D6BBF993EF15F084C/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002E51</idno><idno type="wicri:Area/Main/Curation">002A68</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction</title><author><name sortKey="Kanazawa, Ichiro" sort="Kanazawa, Ichiro" uniqKey="Kanazawa I" first="Ichiro" last="Kanazawa">Ichiro Kanazawa</name><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Kwak, Shin" sort="Kwak, Shin" uniqKey="Kwak S" first="Shin" last="Kwak">Shin Kwak</name><affiliation><mods:affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 113 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Sasaki, Hidenao" sort="Sasaki, Hidenao" uniqKey="Sasaki H" first="Hidenao" last="Sasaki">Hidenao Sasaki</name><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Muramoto, Osamu" sort="Muramoto, Osamu" uniqKey="Muramoto O" first="Osamu" last="Muramoto">Osamu Muramoto</name><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation><wicri:noCountry code="subField">en 305 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Mizutani, Toshio" sort="Mizutani, Toshio" uniqKey="Mizutani T" first="Toshio" last="Mizutani">Toshio Mizutani</name><affiliation><mods:affiliation>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 118 Japan</wicri:noCountry></affiliation></author><author><name sortKey="Hori, Akira" sort="Hori, Akira" uniqKey="Hori A" first="Akira" last="Hori">Akira Hori</name><affiliation><mods:affiliation>Department of Pathology, University of Göttingen, Göttingen F.R.G.</mods:affiliation><wicri:noCountry code="subField">Göttingen F.R.G.</wicri:noCountry></affiliation></author><author><name sortKey="Nukina, Nobuyuki" sort="Nukina, Nobuyuki" uniqKey="Nukina N" first="Nobuyuki" last="Nukina">Nobuyuki Nukina</name><affiliation><mods:affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</mods:affiliation><wicri:noCountry code="subField">Tokyo 113 Japan</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1987">1987</date><biblScope unit="volume">83</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="63">63</biblScope><biblScope unit="page" to="74">74</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">60F8C350DF5B61978A2C138D6BBF993EF15F084C</idno><idno type="DOI">10.1016/0022-510X(88)90020-2</idno><idno type="PII">0022-510X(88)90020-2</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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