Dysfunction of neurotransmitter signalling can cause pathological behaviour similar to that seen in schizophrenia, according to a paper published online in the journal Nature Neuroscience. This finding may prove important for developing future therapeutic targets for disorders associated with psychosis.
Kazu Nakazawa and colleagues created a line of mice that lacked a particular functional receptor for the neurotransmitter glutamate in the inhibitory neurons located in brain regions responsible for cognitive function, emotion and memory. These mice developed various psychotic symptoms including changes in spatial working memory and increased anxiety. However, when the authors engineered the mice so that the receptor dysfunction would not occur until after adolescence, the mice showed no psychosis-like symptoms, suggesting that dysfunction of glutamate signalling specifically during development was responsible for the irregular behaviour.
Although there is thought to be a genetic contribution to schizophrenia, this disorder has not been linked to specific mutations in glutamate receptors. This mouse model aims to specifically test the 'glutamate' hypothesis in schizophrenia, which is based on evidence that various drugs of abuse that affect glutamate signalling also induce a variety of symptoms which are typically seen in schizophrenia, including social withdrawal and psychosis.
Regardless of whether these specific changes in glutamate transmission are found in human patients, this mouse model can be used to understand the changes that lead to psychotic behaviour.
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