Aquaporin 4 differentially modulates osmotic effects on vasopressin neurons in rat supraoptic nucleus.
astrocytes
glial fibrillary acidic protein
hyponatraemia
hypothalamus
neuroendocrine system
Journal
Acta physiologica (Oxford, England)
ISSN: 1748-1716
Titre abrégé: Acta Physiol (Oxf)
Pays: England
ID NLM: 101262545
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
revised:
28
04
2021
received:
04
02
2021
accepted:
06
05
2021
pubmed:
13
5
2021
medline:
24
8
2021
entrez:
12
5
2021
Statut:
ppublish
Résumé
Glial fibrillary acidic protein (GFAP) molecularly associates with aquaporin 4 (AQP4) in astrocytic plasticity. Here, we further examined how AQP4 modulates osmotic effects on vasopressin (VP) neurons in rat supraoptic nucleus (SON) through interactions with GFAP in astrocytes. Brain slices from adult male rats were kept under osmotic stimulation. Western blot, co-immunoprecipitation, immunohistochemistry and patch-clamp recordings were used for analysis of expressions and interactions between GFAP and AQP4, astrocyte-specific proteins in the SON, as well as their influence on VP neuronal activity. Data were analysed using SPSS software. Hyposmotic challenge (HOC) of acute SON slices caused an early (within 5 minutes) and transient increase in the colocalization of AQP4 with GFAP filaments. This effect was prominent at astrocytic processes surrounding VP neuron somata and was accompanied by inhibition of VP neuronal activity. Similar HOC effect was seen in the SON isolated from rats subjected to in vivo HOC, wherein a transiently increased molecular association between GFAP and AQP4 was detected using co-immunoprecipitation. The late stage rebound excitation (10 minutes) of VP neurons in brain slices subjected to HOC and the associated astrocytic GFAP's 'return to normal' were both hampered by 2-(nicotinamide)-1,3,4-thiadiazole, a specific AQP4 channel blocker that itself did not influence VP neuronal activity. Moreover, this agent prevented hyperosmotic stress-evoked excitation of VP neurons and associated reduction in GFAP filaments. These findings indicate that osmotically driven increase in VP neuronal activity requires the activation of AQP4, which determines a retraction of GFAP filaments.
Identifiants
pubmed: 33978309
doi: 10.1111/apha.13672
pmc: PMC8270393
mid: NIHMS1703965
doi:
Substances chimiques
Aqp4 protein, rat
0
Aquaporin 4
0
Vasopressins
11000-17-2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13672Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM123971
Pays : United States
Informations de copyright
© 2021 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.
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