dizocilpine-maleate has been researched along with fasudil* in 2 studies
2 other study(ies) available for dizocilpine-maleate and fasudil
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Antipsychotic-like effects of fasudil, a Rho-kinase inhibitor, in a pharmacologic animal model of schizophrenia.
Current antipsychotics used to treat schizophrenia have associated problems, including serious side effects and treatment resistance. We recently identified a significant association of schizophrenia with exonic copy number variations in the Rho GTPase activating protein 10 (ARHGAP10) gene using genome-wide analysis. ARHGAP10 encodes a RhoGAP superfamily member that is involved in small GTPase signaling. In mice, Arhgap10 gene variations result in RhoA/Rho-kinase pathway activation. We evaluated the pharmacokinetics of fasudil and hydroxyfasudil using liquid chromatography-tandem mass spectrometry in mice. The antipsychotic effects of fasudil on hyperlocomotion, social interaction deficits, prepulse inhibition deficits, and novel object recognition deficits were also investigated in a MK-801-treated pharmacological mouse schizophrenia model. Fasudil and its major metabolite, hydroxyfasudil, were detected in the brain at concentrations above their respective K Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Antipsychotic Agents; Disease Models, Animal; Dizocilpine Maleate; DNA Copy Number Variations; Mice; Protein Kinase Inhibitors; rho-Associated Kinases; Schizophrenia | 2022 |
Nitric oxide: a downstream mediator of calcium toxicity in the ischemic cascade.
Loss of cellular calcium homeostasis or the production of nitric oxide (NO) have been cited as possible mechanisms that may contribute to neuronal degeneration during ischemia. We therefore examined whether cellular calcium blockade, using the agent HA1077, was protective during anoxia in hippocampal neuronal cell cultures, and whether the in vitro effects of this drug were linked to the NO pathway. Administration of the agent during anoxia was neuroprotective in neuronal cell culture. In contrast, HA1077 did not protect hippocampal neurons during NO exposure. In addition, inhibition of NO synthesis in conjunction with HA1077 application during anoxia did not significantly increase survival beyond the maximum protection afforded by HA1077 alone. These results suggest that calcium may be an initial messenger in the ischemic cascade, but that subsequent neuronal degeneration is dependent upon the NO pathway. Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Brain Ischemia; Calcium; Cell Death; Cells, Cultured; Dizocilpine Maleate; Hippocampus; Homeostasis; Isoquinolines; Nitric Oxide; Nitroprusside; Rats; Rats, Sprague-Dawley | 1994 |