Subregional loss of putaminal efferents to the basal ganglia output nuclei may cause parkinsonism in striatonigral degeneration

Satoshi Goto, Sadayuki Matsumoto, Yukitaka Ushio, Asao Hirano

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

In this study, we examined the topographic involvement of the putaminal projection neurons and their axons in the globus pallidus and substantia nigra, which we visualized by calcineurin immunostaining, in the basal ganglia of patients with striatonigral degeneration (SND). In all cases examined, there was a marked decrease in number of calcineurin-immunopositive neurons in the caudal and lateral portion of the putamen. Also, marked depletion of calcineurin-immunoreactive putaminal efferents was consistently present in the posteroventrolateral portions of the globus pallidus interna (GPi) and externa, and in the ventrolateral portion of the substantia nigra pars reticulata (SNr) topographically corresponding to the putaminal lesion. In view of the functional model of the basal ganglia 'motor' circuit, these findings suggest that subregional deafferentation of the GPi/SNr (i.e., basal ganglia output nuclei/from putaminal inputs may be responsible for parkinsonism in patients with SND.

Original languageEnglish (US)
Pages (from-to)1032-1036
Number of pages5
JournalNeurology
Volume47
Issue number4
StatePublished - Oct 1996

Fingerprint

Striatonigral Degeneration
Globus Pallidus
Calcineurin
Parkinsonian Disorders
Basal Ganglia
Neurons
Putamen
Substantia Nigra
Axons
Pars Reticulata

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Subregional loss of putaminal efferents to the basal ganglia output nuclei may cause parkinsonism in striatonigral degeneration. / Goto, Satoshi; Matsumoto, Sadayuki; Ushio, Yukitaka; Hirano, Asao.

In: Neurology, Vol. 47, No. 4, 10.1996, p. 1032-1036.

Research output: Contribution to journalArticle

Goto, Satoshi ; Matsumoto, Sadayuki ; Ushio, Yukitaka ; Hirano, Asao. / Subregional loss of putaminal efferents to the basal ganglia output nuclei may cause parkinsonism in striatonigral degeneration. In: Neurology. 1996 ; Vol. 47, No. 4. pp. 1032-1036.
@article{a1cf819677f84d52b409f277ffd01957,
title = "Subregional loss of putaminal efferents to the basal ganglia output nuclei may cause parkinsonism in striatonigral degeneration",
abstract = "In this study, we examined the topographic involvement of the putaminal projection neurons and their axons in the globus pallidus and substantia nigra, which we visualized by calcineurin immunostaining, in the basal ganglia of patients with striatonigral degeneration (SND). In all cases examined, there was a marked decrease in number of calcineurin-immunopositive neurons in the caudal and lateral portion of the putamen. Also, marked depletion of calcineurin-immunoreactive putaminal efferents was consistently present in the posteroventrolateral portions of the globus pallidus interna (GPi) and externa, and in the ventrolateral portion of the substantia nigra pars reticulata (SNr) topographically corresponding to the putaminal lesion. In view of the functional model of the basal ganglia 'motor' circuit, these findings suggest that subregional deafferentation of the GPi/SNr (i.e., basal ganglia output nuclei/from putaminal inputs may be responsible for parkinsonism in patients with SND.",
author = "Satoshi Goto and Sadayuki Matsumoto and Yukitaka Ushio and Asao Hirano",
year = "1996",
month = "10",
language = "English (US)",
volume = "47",
pages = "1032--1036",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Subregional loss of putaminal efferents to the basal ganglia output nuclei may cause parkinsonism in striatonigral degeneration

AU - Goto, Satoshi

AU - Matsumoto, Sadayuki

AU - Ushio, Yukitaka

AU - Hirano, Asao

PY - 1996/10

Y1 - 1996/10

N2 - In this study, we examined the topographic involvement of the putaminal projection neurons and their axons in the globus pallidus and substantia nigra, which we visualized by calcineurin immunostaining, in the basal ganglia of patients with striatonigral degeneration (SND). In all cases examined, there was a marked decrease in number of calcineurin-immunopositive neurons in the caudal and lateral portion of the putamen. Also, marked depletion of calcineurin-immunoreactive putaminal efferents was consistently present in the posteroventrolateral portions of the globus pallidus interna (GPi) and externa, and in the ventrolateral portion of the substantia nigra pars reticulata (SNr) topographically corresponding to the putaminal lesion. In view of the functional model of the basal ganglia 'motor' circuit, these findings suggest that subregional deafferentation of the GPi/SNr (i.e., basal ganglia output nuclei/from putaminal inputs may be responsible for parkinsonism in patients with SND.

AB - In this study, we examined the topographic involvement of the putaminal projection neurons and their axons in the globus pallidus and substantia nigra, which we visualized by calcineurin immunostaining, in the basal ganglia of patients with striatonigral degeneration (SND). In all cases examined, there was a marked decrease in number of calcineurin-immunopositive neurons in the caudal and lateral portion of the putamen. Also, marked depletion of calcineurin-immunoreactive putaminal efferents was consistently present in the posteroventrolateral portions of the globus pallidus interna (GPi) and externa, and in the ventrolateral portion of the substantia nigra pars reticulata (SNr) topographically corresponding to the putaminal lesion. In view of the functional model of the basal ganglia 'motor' circuit, these findings suggest that subregional deafferentation of the GPi/SNr (i.e., basal ganglia output nuclei/from putaminal inputs may be responsible for parkinsonism in patients with SND.

UR - http://www.scopus.com/inward/record.url?scp=0029805036&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029805036&partnerID=8YFLogxK

M3 - Article

C2 - 8857740

AN - SCOPUS:0029805036

VL - 47

SP - 1032

EP - 1036

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 4

ER -