Mitochondrial dysfunction in chromaffin cells from the R6/1 mouse model of Huntington's disease: Impact on exocytosis and calcium current regulation.
Calcium channels
Chromaffin cells
Exocytosis
Huntington's disease
Mitochondria
R6/1 mouse
Journal
Neurobiology of disease
ISSN: 1095-953X
Titre abrégé: Neurobiol Dis
Pays: United States
ID NLM: 9500169
Informations de publication
Date de publication:
04 2023
04 2023
Historique:
received:
25
10
2022
revised:
08
02
2023
accepted:
15
02
2023
pubmed:
23
2
2023
medline:
23
3
2023
entrez:
22
2
2023
Statut:
ppublish
Résumé
From a pathogenic perspective, Huntington's disease (HD) is being considered as a synaptopathy. As such, alterations in brain neurotransmitter release occur. As the activity of the sympathoadrenal axis is centrally controlled, deficits in the exocytotic release of catecholamine release may also occur. In fact, in chromaffin cells (CCs) of the adrenal medulla of the R6/1 model of HD, decrease of secretion and altered kinetics of the exocytotic fusion pore have been reported. Those alterations could be linked to mitochondrial deficits occurring in peripheral CCs, similar to those described in brain mitochondria. Here we have inquired about alterations in mitochondrial structure and function and their impact on exocytosis and calcium channel currents (I
Identifiants
pubmed: 36806818
pii: S0969-9961(23)00060-8
doi: 10.1016/j.nbd.2023.106046
pii:
doi:
Substances chimiques
Calcium
SY7Q814VUP
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
370-86-5
Catecholamines
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
106046Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.