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article imageMice modeling schizophrenia show key brain network in overdrive Special

By Tim Sandle     Oct 16, 2013 in Science
Using mice genetically engineered to display symptoms of schizophrenia, scientists have uncovered a faulty brain mechanism that may underlie schizophrenia.
Human patients with cognitive disorders such as autism spectrum disorders and schizophrenia show abnormal neural activity in what’s known as the default mode network (DMN). This is a network that is part of the brain structure believed to process memories. It was on this basis that this latest research study was based. In neuroscience, the default mode network is a network of brain regions that are active when the individual is not focused on the outside world and the brain is at wakeful rest.
The Digital Journal was contacted by Juliette Savin (of RIKEN, the natural sciences research institute in Japan) about the research, which was led by Dr. Susumu Tonegawa.
Through the research, the scientists have identified a specific brain network abnormality to schizophrenia, whose symptoms range from disorganized thinking, hallucinations and paranoia to an inability to plan for the future. This came about using a genetically modified mouse with a gene mutation that some schizophrenia patients also harbor. The gene mutation was for a normal gene for an enzyme called calcineurin. This enzyme plays an important role in synaptic plasticity for learning and memory.
The behaviors of mice with the modified genes were compared with unmodified mice. Various mazes and puzzles were set and the ability of the mice to complete the exercises was assessed.
It was found that when rodents run a maze, neurons within the hippocampus exhibit location-specific responses, which are known as ‘place fields’. The hippocampus is the part of the brain that deals with information from short-term memory to long-term memory and spatial navigation.
In normal animals, these location-specific responses are replayed in a series during rest periods following the task performance. However, the genetically altered mice did not reactivate place cells in an ordered manner after the task. The difference was seen as akin to various cognitive disorders.
The implications of the research are that scientists now have a new target for future investigation into the neural basis of a cognitive disorder.
The research was undertaken by neuroscientists at the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory at MIT. The findings will be published in the journal Neuron.
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