Specific neuronal subpopulations in the amygdala of macaque monkeys express high levels of nonphosphorylated neurofilaments.


Journal

Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503

Informations de publication

Date de publication:
15 02 2022
Historique:
received: 31 08 2021
revised: 14 11 2021
accepted: 21 12 2021
pubmed: 28 12 2021
medline: 24 3 2022
entrez: 27 12 2021
Statut: ppublish

Résumé

Pyramidal neurons in the neocortex that express nonphosphorylated neurofilaments (NPNFs) are especially vulnerable to degeneration in Alzheimer's disease. Since the basolateral nuclear complex of the amygdala (BNC) and cortical nuclear complex of the amygdala (CNC) are cortex-like structures, containing both pyramidal (PNs) and nonpyramidal neurons (NPNs), it is of interest to determine which cell types in the primate BNC and CNC are NPNF+. We also studied NPNF expression in the non-cortex-like nuclei of the amygdala (central and medial nuclei). Digitized images of sections through fetal, newborn, infant, and adult macaque brains stained for NPNFs, obtained from the Macaque Brain Resource (MacBrainResource, MBR), were analyzed. The pattern of NPNF immunoreactivity (NPNF-ir) in the BNC, CNC, and medial nucleus was essentially identical in all four age groups, but there were some age-dependent differences in the central nucleus. All BNC and CNC nuclei contained a moderate density of NPNF+ NPNs. Both the somata and the entire dendritic arborizations of these NPNs were stained. PNs with robust NPNF-ir in their somata and proximal dendrites were only seen in the basal magnocellular nucleus, where it appeared that virtually every PN was NPNF+. This pattern of NPNF expression is distinct from that seen in the mammalian neocortex, where NPNF+ neurons are almost entirely PNs, but is very similar to that seen in a recent study of the rat BNC. These findings, in conjunction with the cortical data, suggest the possibility that NPNF+ neuronal subpopulations in the BNC and CNC might be especially vulnerable in Alzheimer's disease.

Identifiants

pubmed: 34958755
pii: S0006-8993(21)00626-0
doi: 10.1016/j.brainres.2021.147767
pmc: PMC8792357
mid: NIHMS1767868
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

147767

Subventions

Organisme : NIMH NIH HHS
ID : R01 MH104638
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH113257
Pays : United States

Informations de copyright

Copyright © 2021 Elsevier B.V. All rights reserved.

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Auteurs

Alexander Joseph McDonald (AJ)

Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, SC 29208, USA. Electronic address: alexander.mcdonald@uscmed.sc.edu.

Alvaro Duque (A)

Department of Neuroscience, Yale University School of Medicine, SHM C317B, New Haven, CT 06520, USA.

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Classifications MeSH