Anti-NMDAR1 antibody impairs dendritic branching in immature cultured neurons

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F24%3A43921331" target="_blank" >RIV/00023752:_____/24:43921331 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11120/24:43927546

Výsledek na webu

<a href="https://jab.zsf.jcu.cz/artkey/jab-202403-0003_anti-nmdar1-antibody-impairs-dendritic-branching-in-immature-cultured-neurons.php" target="_blank" >https://jab.zsf.jcu.cz/artkey/jab-202403-0003_anti-nmdar1-antibody-impairs-dendritic-branching-in-immature-cultured-neurons.php</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.32725/jab.2024.019" target="_blank" >10.32725/jab.2024.019</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Anti-NMDAR1 antibody impairs dendritic branching in immature cultured neurons

Popis výsledku v původním jazyce

Anti-N N-methyl D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune disorder characterized by IgG antibodies targeting NMDAR. The prevalence is remarkably higher in women and some develop the condition during pregnancy. While immunotherapies have shown good outcomes for pregnant mothers and their infants, the impact on early neurodevelopment remains elusive. This study investigates the effects of anti-NMDAR antibody on the development of primary cortical cultures. Anti-NMDAR antibody was administered to the cultures at day in vitro 5 for the following 5 days to assess dendritic branching and arbor complexity, and at day in vitro 14 for measuring the expression of brain-derived neurotrophic factor (BDNF) and synaptic proteins. Immature cultured neurons treated with anti-NMDAR antibody exhibited impaired dendritic branching and arbor complexity. Interestingly, BDNF expression was unaffected in mature neurons. Additionally, GluN1 expression, a mandatory NMDAR subunit, was significantly reduced, while no significant alterations were observed in PSD-95, gephyrin and synaptophysin expression. These findings shed light on the structural and synaptic impacts of anti-NMDAR antibody on immature neurons, providing evidence for their consequences in early neuronal development.

Název v anglickém jazyce

Anti-NMDAR1 antibody impairs dendritic branching in immature cultured neurons

Popis výsledku anglicky

Anti-N N-methyl D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune disorder characterized by IgG antibodies targeting NMDAR. The prevalence is remarkably higher in women and some develop the condition during pregnancy. While immunotherapies have shown good outcomes for pregnant mothers and their infants, the impact on early neurodevelopment remains elusive. This study investigates the effects of anti-NMDAR antibody on the development of primary cortical cultures. Anti-NMDAR antibody was administered to the cultures at day in vitro 5 for the following 5 days to assess dendritic branching and arbor complexity, and at day in vitro 14 for measuring the expression of brain-derived neurotrophic factor (BDNF) and synaptic proteins. Immature cultured neurons treated with anti-NMDAR antibody exhibited impaired dendritic branching and arbor complexity. Interestingly, BDNF expression was unaffected in mature neurons. Additionally, GluN1 expression, a mandatory NMDAR subunit, was significantly reduced, while no significant alterations were observed in PSD-95, gephyrin and synaptophysin expression. These findings shed light on the structural and synaptic impacts of anti-NMDAR antibody on immature neurons, providing evidence for their consequences in early neuronal development.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30104 - Pharmacology and pharmacy

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2024

Kód důvěrnosti údajů

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

Název periodika

Journal of Applied Biomedicine

ISSN

1214-021X

e-ISSN

1214-0287

Svazek periodika

22

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

5

Strana od-do

136-140

Kód UT WoS článku

001318034300001

EID výsledku v databázi Scopus

2-s2.0-85206960900