Thesis
A MAP2K7 genetic mouse model as an investigative tool of the cognitive and behavioural deficits in schizophrenia
- Creator
- Rights statement
- Awarding institution
- University of Strathclyde
- Date of award
- 2013
- Thesis identifier
- T13640
- Qualification Level
- Qualification Name
- Department, School or Faculty
- Abstract
- Schizophrenia is a devastating psychiatric disease affected by multiple factors, such as genetic, environmental and social. This study suggests a strong genetic contribution of the MAP2K7 candidate gene in risk for schizophrenia. It was reported earlier that the expression of MKK7/MAP2K7 kinase activated by glutamatergic activity is decreased in the post-mortem PFC from patients with schizophrenia, suggesting that reduced function of the MAP2K7-c-Jun N-terminal kinase (JNK) signalling cascade may offer an insight of neurochemical changes in schizophrenia. Current study investigates MAP2K7 heterozygous mice and suggests a schizophrenia-like cognitive phenotype of impaired working memory with a use of 8 radial arm maze and the n-back short-term memory performance task. Study also shows that potent NMDA-receptor antagonist ketamine treatment induces some alterations in the cerebral glucose uptake in the various brain regions and produces hypometabolism, however this pattern could be observed in both wild-type and MAP2K7 heterozygous mice. Therefore, the study introduces new evidence of altered expression of MAP2K7 gene and its effect on short-term working memory in mice, as well as ketamine-induced alterations of cerebral glucose uptake in numerous regions of the mice brain.
- Resource Type
- DOI
- Date Created
- 2013
- Former identifier
- 1004587