Models of schizophrenia in humans and animals based on inhibition of NMDA receptors
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
18471877
DOI
10.1016/j.neubiorev.2008.03.012
PII: S0149-7634(08)00050-X
Knihovny.cz E-zdroje
- MeSH
- antagonisté excitačních aminokyselin farmakologie MeSH
- fyziologická adaptace MeSH
- ketamin farmakologie MeSH
- lidé MeSH
- modely nemocí na zvířatech MeSH
- modely neurologické MeSH
- receptory N-methyl-D-aspartátu antagonisté a inhibitory metabolismus MeSH
- schizofrenie metabolismus patofyziologie MeSH
- toxické psychózy metabolismus patofyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- antagonisté excitačních aminokyselin MeSH
- ketamin MeSH
- receptory N-methyl-D-aspartátu MeSH
The research of the glutamatergic system in schizophrenia has advanced with the use of non-competitive antagonists of glutamate NMDA receptors (phencyclidine, ketamine, and dizocilpine), which change both human and animal behaviour and induce schizophrenia-like manifestations. Models based on both acute and chronic administration of these substances in humans and rats show phenomenological validity and are suitable for searching for new substances with antipsychotic effects. Nevertheless, pathophysiology of schizophrenia remains unexplained. In the light of the neurodevelopmental model of schizophrenia based on early administration of NMDA receptor antagonists it seems that increased cellular destruction by apoptosis or changes in function of glutamatergic NMDA receptors in the early development of central nervous system are decisive for subsequent development of psychosis, which often does not manifest itself until adulthood. Chronic administration of antagonists initializes a number of adaptation mechanisms, which correlate with findings obtained in patients with schizophrenia; therefore, this model is also suitable for research into pathophysiology of this disease.
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