Neuronal localization of m1 muscarinic receptor immunoreactivity in the monkey basolateral amygdala.


Journal

The Journal of comparative neurology
ISSN: 1096-9861
Titre abrégé: J Comp Neurol
Pays: United States
ID NLM: 0406041

Informations de publication

Date de publication:
01 07 2021
Historique:
revised: 17 12 2020
received: 27 10 2020
accepted: 01 01 2021
pubmed: 8 1 2021
medline: 1 2 2022
entrez: 7 1 2021
Statut: ppublish

Résumé

The basolateral nuclear complex (BNC) of the amygdala plays an important role in the generation of emotional/motivational behavior and the consolidation of emotional memories. Activation of M1 cholinergic receptors (M1Rs) in the BNC is critical for memory consolidation. Previous receptor binding studies in the monkey amygdala demonstrated that the BNC has a high density of M1Rs, but did not have sufficient resolution to identify which neurons in the BNC expressed them. This was accomplished in the present immunohistochemical investigation using an antibody for the m1 receptor (m1R). Analysis of m1Rs in the monkey BNC using immunoperoxidase techniques revealed that their expression was very dense in the BNC, and suggested that virtually all of the pyramidal projection neurons (PNs) in all of the BNC nuclei were m1R-immunoreactive (m1R+). This was confirmed with dual-labeling immunofluorescence using staining for calcium/calmodulin-dependent protein kinase II (CaMK) as a marker for BNC PNs. However, additional dual-labeling studies indicated that one-third of inhibitory interneurons (INs) expressing glutamic acid decarboxylase (GAD) were also m1R+. Moreover, the finding that 60% of parvalbumin (PV) immunoreactive neurons were m1R+ indicated that this IN subpopulation was the main GAD+ subpopulation exhibiting m1R expression. The cholinergic innervation of the amygdala is greatly reduced in Alzheimer's disease and there is currently considerable interest in developing selective M1R positive allosteric modulators (PAMs) to treat the symptoms. The results of the present study indicate that M1Rs in both PNs and INs in the primate BNC would be targeted by M1R PAMs.

Identifiants

pubmed: 33410202
doi: 10.1002/cne.25104
pmc: PMC8113068
mid: NIHMS1659875
doi:

Substances chimiques

Receptor, Muscarinic M1 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2450-2463

Subventions

Organisme : NIH HHS
ID : P51 OD011132
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH104638
Pays : United States
Organisme : NIH HHS
ID : P51OD011132
Pays : United States
Organisme : NIMH NIH HHS
ID : R01MH104638
Pays : United States

Informations de copyright

© 2021 Wiley Periodicals LLC.

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Auteurs

Alexander Joseph McDonald (AJ)

Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, South Carolina, USA.

David D Mott (DD)

Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, South Carolina, USA.

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Classifications MeSH