The disruption of circadian rhythmicity of gene expression in the hippocampus and associated structures in Gria2R/R mice, a comparison with C57BL/6J and Adar2−/− mice strains

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00583680" target="_blank" >RIV/67985823:_____/24:00583680 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11310/24:10476692 RIV/00023752:_____/24:43921323

Výsledek na webu

<a href="https://doi.org/10.1016/j.brainres.2023.148739" target="_blank" >https://doi.org/10.1016/j.brainres.2023.148739</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.brainres.2023.148739" target="_blank" >10.1016/j.brainres.2023.148739</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The disruption of circadian rhythmicity of gene expression in the hippocampus and associated structures in Gria2R/R mice, a comparison with C57BL/6J and Adar2−/− mice strains

Popis výsledku v původním jazyce

Adar2-/- mice are a widely used model for studying the physiological consequences of reduced RNA editing. These mice are viable only when the Q/R editing site of the Gria2 subunit of the AMPA receptor is constitutively mutated to the codon for arginine, and Gria2R/R mice often serve as the sole control for Adar2-/- mice. Our study aimed to investigate whether ADAR2 inactivity and the Gria2R/R phenotype affect the rhythmicity of the circadian clock gene pattern and the expression of Gria1 and Gria2 subunits in the suprachiasmatic nucleus (SCN), hippocampus, parietal cortex and liver. Our data show that Gria2R/R mice completely lost circadian rhythmicity in the hippocampus compared to Adar2-/- mice. Compared to C57BL/6J mice, the expression profiles in the hippocampus and parietal cortex of Gria2R/R mice differ to the same extent as in Adar2-/-. No alterations were detected in the circadian profiles in the livers. These data suggest that the natural gradual postnatal increase in the editing of the Q/R site of the Gria2 subunit may be important for the development of circadian clockwork in some brain structures, and the use of Gria2R/R mice as the only control to Adar2-/- mice in the experiments dependent on the hippocampus and parietal cortex should therefore be considered.

Název v anglickém jazyce

The disruption of circadian rhythmicity of gene expression in the hippocampus and associated structures in Gria2R/R mice, a comparison with C57BL/6J and Adar2−/− mice strains

Popis výsledku anglicky

Adar2-/- mice are a widely used model for studying the physiological consequences of reduced RNA editing. These mice are viable only when the Q/R editing site of the Gria2 subunit of the AMPA receptor is constitutively mutated to the codon for arginine, and Gria2R/R mice often serve as the sole control for Adar2-/- mice. Our study aimed to investigate whether ADAR2 inactivity and the Gria2R/R phenotype affect the rhythmicity of the circadian clock gene pattern and the expression of Gria1 and Gria2 subunits in the suprachiasmatic nucleus (SCN), hippocampus, parietal cortex and liver. Our data show that Gria2R/R mice completely lost circadian rhythmicity in the hippocampus compared to Adar2-/- mice. Compared to C57BL/6J mice, the expression profiles in the hippocampus and parietal cortex of Gria2R/R mice differ to the same extent as in Adar2-/-. No alterations were detected in the circadian profiles in the livers. These data suggest that the natural gradual postnatal increase in the editing of the Q/R site of the Gria2 subunit may be important for the development of circadian clockwork in some brain structures, and the use of Gria2R/R mice as the only control to Adar2-/- mice in the experiments dependent on the hippocampus and parietal cortex should therefore be considered.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2024

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Brain Research

ISSN

0006-8993

e-ISSN

1872-6240

Svazek periodika

1826

Číslo periodika v rámci svazku

1 March

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

5

Strana od-do

148739

Kód UT WoS článku

001165646600001

EID výsledku v databázi Scopus

2-s2.0-85181063268