Too much of the  NOS1AP protein resulted in the dendrites - tree-like structures that allow cells to talk to each other and are essential to the functioning of the nervous system - being stunted in the developing brains of rats, the researchers found.

"When the brain develops, it sets up a system of the right type of connectivity to make sure that communication can occur," said Bonnie Firestein from the Rutgers University in the US.

"What we saw here was that the nerve cells did not move to the correct locations and did not have dendrites that branch out to make the connections that were needed,"  Firestein added.

The researchers found that too much of the NOS1AP protein in brain cells did not allow them to branch out and kept them deep within the neo-cortex, the portion of the brain responsible for higher functioning skills, such as spatial reasoning, conscious thought, motor commands, language development and sensory perception.

In the control group of rats in which the NOS1AP protein was not over-expressed, the cellular connections developed properly, with cells moving out to the outer layers of the neocortex and enabling the nerve cells to communicate.

Although scientists cannot pinpoint for certain the exact cause of schizophrenia, they have determined that several genes, including NOS1AP, are associated with an increased risk for the disabling brain disorder. The study appeared in the journal Biological Psychiatry.

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