Neuron types in the primate striatum: Stereological analysis of projection neurons and interneurons in control and parkinsonian monkeys.


Journal

Neuropathology and applied neurobiology
ISSN: 1365-2990
Titre abrégé: Neuropathol Appl Neurobiol
Pays: England
ID NLM: 7609829

Informations de publication

Date de publication:
08 2022
Historique:
revised: 08 02 2022
received: 20 08 2021
accepted: 12 02 2022
pubmed: 12 3 2022
medline: 7 7 2022
entrez: 11 3 2022
Statut: ppublish

Résumé

The striatum is mainly composed of projection neurons. It also contains interneurons, which modulate and control striatal output. The aim of the present study was to assess the percentages of projection neurons and interneuron populations in the striatum of control monkeys and of parkinsonian monkeys. Unbiased stereology was used to estimate the volume density of every neuron population in the caudate, putamen and ventral striatum of control monkeys and of monkeys treated with MPTP, which results in striatal dopamine depletion. The various neuron population phenotypes were identified by immunohistochemistry. All analyses were performed within the same subjects using similar processing and analysis parameters, thus allowing for reliable data comparisons. In control monkeys, the projection neurons, which express the dopamine-and-cAMP-regulated-phosphoprotein, 32-KDa (DARPP-32), were the most abundant: ~86% of the total neurons counted. The interneurons accounted for the remaining 14%. Among the interneurons, those expressing calretinin were the most abundant (Cr+: ~57%; ~8% of the total striatal neurons counted), followed those expressing Parvalbumin (Pv+: ~18%; 2.6%), dinucleotide phosphate-diaphorase (NADPH+: ~13%; 1.8%), choline acetyltransferase (ChAT+: ~11%; 1.5%) and tyrosine hydroxylase (TH+: ~0.5%; 0.1%). No significant changes in volume densities occurred in any population following dopamine depletion, except for the TH+ interneurons, which increased in parkinsonian non-symptomatic monkeys and even more in symptomatic monkeys. These data are relevant for translational studies targeting specific neuron populations of the striatum. The fact that dopaminergic denervation does not cause neuron loss in any population has potential pathophysiological implications.

Identifiants

pubmed: 35274336
doi: 10.1111/nan.12812
doi:

Substances chimiques

Dopamine VTD58H1Z2X

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e12812

Informations de copyright

© 2022 The Authors. Neuropathology and Applied Neurobiology published by John Wiley & Sons Ltd on behalf of British Neuropathological Society.

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Auteurs

Natalia López-González Del Rey (NL)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
CIBERNED (Center for Networked Biomedical Research on Neurodegenerative Diseases), Instituto Carlos III, Madrid, Spain.
PhD Program in Neuroscience Autónoma de Madrid University-Cajal Institute, Madrid, Spain.

Inés Trigo-Damas (I)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
CIBERNED (Center for Networked Biomedical Research on Neurodegenerative Diseases), Instituto Carlos III, Madrid, Spain.

José A Obeso (JA)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
CIBERNED (Center for Networked Biomedical Research on Neurodegenerative Diseases), Instituto Carlos III, Madrid, Spain.

Carmen Cavada (C)

PhD Program in Neuroscience Autónoma de Madrid University-Cajal Institute, Madrid, Spain.
Department of Anatomy, Histology and Neuroscience, School of Medicine, Autónoma de Madrid University, Madrid, Spain.

Javier Blesa (J)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
CIBERNED (Center for Networked Biomedical Research on Neurodegenerative Diseases), Instituto Carlos III, Madrid, Spain.

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