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Statements

Subject Item
n2:RIV%2F00023752%3A_____%2F03%3A00000323%21RIV%2F2004%2FMZ0%2FL28004%2FN
rdf:type
n14:Vysledek skos:Concept
dcterms:description
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. 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.
dcterms:title
Viral infection, glutamatergic deficit and behavioral changes in animal model of schizophrenia Viral infection, glutamatergic deficit and behavioral changes in animal model of schizophrenia
skos:prefLabel
Viral infection, glutamatergic deficit and behavioral changes in animal model of schizophrenia Viral infection, glutamatergic deficit and behavioral changes in animal model of schizophrenia
skos:notation
RIV/00023752:_____/03:00000323!RIV/2004/MZ0/L28004/N
n3:strany
128-130
n3:aktivita
n13:P
n3:aktivity
P(NF6031), P(NF7626)
n3:cisloPeriodika
Suppl. 2
n3:dodaniDat
n10:2004
n3:domaciTvurceVysledku
n4:6507026 n4:3712869 n4:6898645
n3:druhVysledku
n9:J
n3:duvernostUdaju
n7:S
n3:entitaPredkladatele
n17:predkladatel
n3:idSjednocenehoVysledku
633033
n3:idVysledku
RIV/00023752:_____/03:00000323
n3:jazykVysledku
n16:eng
n3:klicovaSlova
schizophrenia; animal model; quinolinic acid; NMDA receptor; dopamine; haloperidol; clozapine; acoustic startle reaction; prepulse inhibition; open field test
n3:klicoveSlovo
n5:acoustic%20startle%20reaction n5:animal%20model n5:open%20field%20test n5:clozapine n5:haloperidol n5:prepulse%20inhibition n5:schizophrenia n5:quinolinic%20acid n5:dopamine n5:NMDA%20receptor
n3:kodStatuVydavatele
CZ - Česká republika
n3:kontrolniKodProRIV
[72944537B4D7]
n3:nazevZdroje
Psychiatrie
n3:obor
n6:FH
n3:pocetDomacichTvurcuVysledku
3
n3:pocetTvurcuVysledku
4
n3:pocetUcastnikuAkce
0
n3:pocetZahranicnichUcastnikuAkce
0
n3:projekt
n15:NF6031 n15:NF7626
n3:rokUplatneniVysledku
n10:2003
n3:svazekPeriodika
7
n3:tvurceVysledku
Balcar, Vladimír Joseph Höschl, Cyril Šťastný, František Tejkalová, Hana
s:issn
1211-7579
s:numberOfPages
3