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Schizophrenia mouse model should improve understanding and treatment of the disorder
Date:12/28/2009

nterneurons that supply GABA to pyramidal cells. "If we take out ErbB4 in these two interneurons, the neuregulin should have no effect because it can't promote GABA," Dr. Mei, Georgia Research Alliance Eminent Scholar in Neuroscience, said.

His postulation played out in the behavior of the mouse, who exhibited schizophrenia-like behavior including increased movement and impaired short-term memory. The scientists are still gathering data on the manic aspect of schizophrenia in their mice.

For example, both the normal and knockout mice learned they would find a food pellet in each arm of an eight-armed chamber but that if they went to the same arm for seconds, there were none. But the knockouts took longer to learn and finish the task. Knockouts also spent a lot more time sniffing and snooping around and revisiting empty arms.

In another test, knockouts couldn't or wouldn't - make the connection that a relatively low noise would be followed by a slightly louder one. When they treated the knockouts with diazepam, an anti-anxiety medication, they responded similarly to the normal mice: the first sound prepared them for the second.

Dr. Mei suspects that if he could look at the chandelier and basket interneurons in the prefrontal cortex of schizophrenics, he would also find something wrong with their usual role of sensing the need for the inhibitor GABA and supplying it to the pyramidal cells. "In schizophrenia, the baseline of the excitatory neurotransmitter is probably high," he said.


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Contact: Toni Baker
tbaker@mcg.edu
706-721-4421
Medical College of Georgia
Source:Eurekalert  

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