期刊
BIOMOLECULES
卷 10, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/biom10060947
关键词
NMDA; depression; schizophrenia; subunit; glutamate; GABA
资金
- Instituto de Salud Carlos III, Subdireccion General de Evaluacion y Fomento de la Investigacion (FIS Grants) - European Regional Development Fund ('A way to build Europe') [PI16/00217, PI19/00170]
- Centro de Investigacion Biomedica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III
- CSIC Open Access Publication Support Initiative through its Unit of Information Resources for Research (URICI)
N-methyl-D-aspartate (NMDA) receptor antagonists such as phencyclidine (PCP), dizocilpine (MK-801) and ketamine have long been considered a model of schizophrenia, both in animals and humans. However, ketamine has been recently approved for treatment-resistant depression, although with severe restrictions. Interestingly, the dosage in both conditions is similar, and positive symptoms of schizophrenia appear before antidepressant effects emerge. Here, we describe the temporal mechanisms implicated in schizophrenia-like and antidepressant-like effects of NMDA blockade in rats, and postulate that such effects may indicate that NMDA receptor antagonists induce similar mechanistic effects, and only the basal pre-drug state of the organism delimitates the overall outcome. Hence, blockade of NMDA receptors in depressive-like status can lead to amelioration or remission of symptoms, whereas healthy individuals develop psychotic symptoms and schizophrenia patients show an exacerbation of these symptoms after the administration of NMDA receptor antagonists.
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