FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2005459453> ?p ?o ?g. }

• W2005459453 endingPage "116" @default.
• W2005459453 startingPage "107" @default.
• W2005459453 abstract "Schizophrenia is a chronic debilitating psychiatric disorder affecting as many as 1% of the population worldwide. Unfortunately, its etiology and pathophysiology are poorly defined. Previous studies have shown that neuronal injury and microglia activation were observed in the schizophrenic patients. The present study aims to evaluate the role of neurons and microglia in ketamine-induced experimental schizophrenic model to further understand its pathophysiology. Firstly, ketamine was used to simulate the behavior abnormalities associated with schizophrenia. The effects of ketamine on mouse locomotor activity, Y-maze task, novel object recognition, and forced swimming test were studied. The results showed that ketamine (25, 50, and 100 mg/kg i.p.) administered acutely or repeatedly (for 7 days) can increase the locomotor number significantly. In Y-maze task, ketamine (25, 50, and 100 mg/kg) impaired spontaneous alternation after both acute and repeated treatments. In novel object recognition test, acute or chronic ketamine treatment showed no significant effect on mouse exploratory preference behavior. In forced swimming test, repeated treatment of ketamine (100 mg/kg) enhanced the immobility duration. Secondly, immunohistochemical method was used to study the changes of neurons and microglia. The results showed that acute treatment of ketamine (100 mg/kg) had no effect on neurons in the prefrontal cortex or hippocampus (1, 3, 5, and 7 days after the treatment). In contrast, repeated treatment of ketamine caused neuronal impairment in mouse hippocampus (3rd day, 5th day and 7th day after the final administration). The results of immunohistochemistry demonstrated that microglia in the prefrontal cortex and hippocampus were not affected after acute or repeated administration of ketamine. Finally, the neuronal impairment caused by repeated administration of ketamine was further investigated from the oxidative stress aspects. The results showed that repeated administration of ketamine increased nitric oxide (NO) and nitric oxide synthase (NOS) in prefrontal cortex, hippocampus and serum, while decreased SOD in hippocampus and serum. In summary, chronic ketamine treatment to mice successfully mimics the core behavioral deficits in schizophrenia. It is demonstrated for the first time that neuronal injury was associated with the chronic ketamine-induced experimental schizophrenic model, while microglial cells may play little role in this model. Oxidative stress may contribute to the significant neuronal injury in mouse brain induced by chronic ketamine treatment." @default.
• W2005459453 created "2016-06-24" @default.
• W2005459453 creator A5022745294 @default.
• W2005459453 creator A5037752888 @default.
• W2005459453 creator A5038884367 @default.
• W2005459453 creator A5052943350 @default.
• W2005459453 creator A5054499629 @default.
• W2005459453 creator A5057336191 @default.
• W2005459453 creator A5062416906 @default.
• W2005459453 creator A5065819734 @default.
• W2005459453 creator A5085925694 @default.
• W2005459453 date "2013-08-01" @default.
• W2005459453 modified "2023-10-17" @default.
• W2005459453 title "Neuronal injury, but not microglia activation, is associated with ketamine-induced experimental schizophrenic model in mice" @default.
• W2005459453 cites W1924622891 @default.
• W2005459453 cites W1964579257 @default.
• W2005459453 cites W1965707086 @default.
• W2005459453 cites W1978238793 @default.
• W2005459453 cites W1980763349 @default.
• W2005459453 cites W1983729020 @default.
• W2005459453 cites W1985836432 @default.
• W2005459453 cites W1986998880 @default.
• W2005459453 cites W1990661023 @default.
• W2005459453 cites W1999555301 @default.
• W2005459453 cites W2010543372 @default.
• W2005459453 cites W2012520574 @default.
• W2005459453 cites W2015246589 @default.
• W2005459453 cites W2018457415 @default.
• W2005459453 cites W2018838561 @default.
• W2005459453 cites W2020140782 @default.
• W2005459453 cites W2023780060 @default.
• W2005459453 cites W2028531603 @default.
• W2005459453 cites W2028884770 @default.
• W2005459453 cites W2032430743 @default.
• W2005459453 cites W2037749055 @default.
• W2005459453 cites W2044004700 @default.
• W2005459453 cites W2044097496 @default.
• W2005459453 cites W2049728523 @default.
• W2005459453 cites W2054002536 @default.
• W2005459453 cites W2057476473 @default.
• W2005459453 cites W2063361808 @default.
• W2005459453 cites W2063765492 @default.
• W2005459453 cites W2064678154 @default.
• W2005459453 cites W2071151533 @default.
• W2005459453 cites W2072441360 @default.
• W2005459453 cites W2074096568 @default.
• W2005459453 cites W2076454433 @default.
• W2005459453 cites W2079772279 @default.
• W2005459453 cites W2081569033 @default.
• W2005459453 cites W2084148205 @default.
• W2005459453 cites W2090905052 @default.
• W2005459453 cites W2091456872 @default.
• W2005459453 cites W2091505284 @default.
• W2005459453 cites W2091855875 @default.
• W2005459453 cites W2093248761 @default.
• W2005459453 cites W2094007274 @default.
• W2005459453 cites W2094660277 @default.
• W2005459453 cites W2094905804 @default.
• W2005459453 cites W2103127225 @default.
• W2005459453 cites W2108610913 @default.
• W2005459453 cites W2112880160 @default.
• W2005459453 cites W2115821201 @default.
• W2005459453 cites W2124433160 @default.
• W2005459453 cites W2127946463 @default.
• W2005459453 cites W2141787834 @default.
• W2005459453 cites W2146264275 @default.
• W2005459453 cites W2150174494 @default.
• W2005459453 cites W2158137297 @default.
• W2005459453 cites W2168928905 @default.
• W2005459453 doi "https://doi.org/10.1016/j.pnpbp.2013.04.006" @default.
• W2005459453 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23603358" @default.
• W2005459453 hasPublicationYear "2013" @default.
• W2005459453 type Work @default.
• W2005459453 sameAs 2005459453 @default.
• W2005459453 citedByCount "46" @default.
• W2005459453 countsByYear W20054594532013 @default.
• W2005459453 countsByYear W20054594532014 @default.
• W2005459453 countsByYear W20054594532015 @default.
• W2005459453 countsByYear W20054594532016 @default.
• W2005459453 countsByYear W20054594532017 @default.
• W2005459453 countsByYear W20054594532018 @default.
• W2005459453 countsByYear W20054594532019 @default.
• W2005459453 countsByYear W20054594532020 @default.
• W2005459453 countsByYear W20054594532021 @default.
• W2005459453 countsByYear W20054594532022 @default.
• W2005459453 countsByYear W20054594532023 @default.
• W2005459453 crossrefType "journal-article" @default.
• W2005459453 hasAuthorship W2005459453A5022745294 @default.
• W2005459453 hasAuthorship W2005459453A5037752888 @default.
• W2005459453 hasAuthorship W2005459453A5038884367 @default.
• W2005459453 hasAuthorship W2005459453A5052943350 @default.
• W2005459453 hasAuthorship W2005459453A5054499629 @default.
• W2005459453 hasAuthorship W2005459453A5057336191 @default.
• W2005459453 hasAuthorship W2005459453A5062416906 @default.
• W2005459453 hasAuthorship W2005459453A5065819734 @default.
• W2005459453 hasAuthorship W2005459453A5085925694 @default.
• W2005459453 hasConcept C118552586 @default.
• W2005459453 hasConcept C126322002 @default.

• next