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Dizocilpine Does Not Alter NOS1AP Gene Expression in Rats and in Cell Cultures
Anton B Matiiv1, Tatyana M Rogoza1,2, Irina A Razgovorova3
1Department of Genetics and Biotechnology, St. Petersburg State University, 7/9 Universitetskaya emb., St. Petersburg 199034, Russia.
International Journal of Molecular Sciences
|June 13, 2025
Summary
Dizocilpine, an NMDA receptor antagonist, did not alter NOS1AP gene expression or protein production in rat models or cell lines. This finding is relevant for understanding schizophrenia
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- The NOS1AP gene encodes a protein that regulates nitric oxide (NO) production by interacting with neuronal nitric oxide synthase (nNOS) and NMDA receptors (NMDARs).
- NOS1AP expression increases with NMDAR activation, but its response to NMDAR inhibition is unknown.
- The NOS1AP gene is implicated in schizophrenia, and NMDAR antagonists like dizocilpine are used in animal models of the disorder.
Purpose of the Study:
- To investigate the effect of dizocilpine (MK-801) on NOS1AP gene expression and protein production.
- To examine NOS1AP regulation under conditions of NMDAR inhibition in both in vivo and in vitro models.
Main Methods:
- Rats were injected with a low dose of dizocilpine (0.1 mg/kg).
- SH-SY5Y and HEK293T cell lines were treated with varying concentrations of dizocilpine (10-200 µM).
- Gene expression and protein production of NOS1AP were analyzed in treated samples.
Main Results:
- Dizocilpine treatment did not significantly affect NOS1AP gene expression in rats or cell lines.
- No changes in NOS1AP protein production were observed following dizocilpine administration.
- The study found no impact of NMDAR inhibition on NOS1AP levels.
Conclusions:
- Dizocilpine, a commonly used NMDAR antagonist, does not alter NOS1AP expression or production.
- These findings suggest that NOS1AP regulation is independent of NMDAR activity under the tested conditions.
- This research provides novel insights into the molecular mechanisms potentially relevant to schizophrenia.

