Viral infection, glutamatergic deficit and behavioral changes in animal model of schizophrenia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F03%3A00000323" target="_blank" >RIV/00023752:_____/03:00000323 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Viral infection, glutamatergic deficit and behavioral changes in animal model of schizophrenia

Popis výsledku v původním jazyce

Retroviruses can disrupt brain development, cause neuronal death and induce behavioural changes and therefore they have been proposed to play a role in the etiology of schizophrenia. Quinolinic acid (QUIN), released from retrovirus-infected brain macrophages and microglia, might be responsible, at least in part, for most of the proposed alterations. Intracerebroventricular infusion of QUIN to rat pups did cause a neuronal damage and evoked a subsequent diminution of the specific membrane binding of glutamate and changed their exploratory and acoustic startle activities in early adulthood. The changes were modified (potentiated) by increased levels of brain dopamine and inhibited by haloperidol and clozapine. Our present data suggest that increased levels of QUIN in neonatal rat brain can induce changes in the brain development and function have effects that exhibit some similarities to human schizophrenia.

Název v anglickém jazyce

Viral infection, glutamatergic deficit and behavioral changes in animal model of schizophrenia

Popis výsledku anglicky

Retroviruses can disrupt brain development, cause neuronal death and induce behavioural changes and therefore they have been proposed to play a role in the etiology of schizophrenia. Quinolinic acid (QUIN), released from retrovirus-infected brain macrophages and microglia, might be responsible, at least in part, for most of the proposed alterations. Intracerebroventricular infusion of QUIN to rat pups did cause a neuronal damage and evoked a subsequent diminution of the specific membrane binding of glutamate and changed their exploratory and acoustic startle activities in early adulthood. The changes were modified (potentiated) by increased levels of brain dopamine and inhibited by haloperidol and clozapine. Our present data suggest that increased levels of QUIN in neonatal rat brain can induce changes in the brain development and function have effects that exhibit some similarities to human schizophrenia.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FH - Neurologie, neurochirurgie, neurovědy

OECD FORD obor

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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

2003

Kód důvěrnosti údajů

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

Název periodika

Psychiatrie

ISSN

1211-7579

e-ISSN

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Svazek periodika

7

Číslo periodika v rámci svazku

Suppl. 2

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

3

Strana od-do

128-130

Kód UT WoS článku

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EID výsledku v databázi Scopus

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