An American study has shed some light on how microscopic changes to brain cause schizophrenia.
"We found several microscopic pathologies and behavioral traits that are hallmarks of schizophrenia. These findings in mice may help shed light on how schizophrenia, an often severe and debilitating disease, emerges in humans," says Dr. Ulrich Mueller, a professor at Scripps Research, who was senior author of the study published in the journal Proceedings of the National Academy of Sciences.
Working in collaboration with Research Associate Claudia Barros, Mueller's team found that the schizophrenic mice could recover normal behaviour when treated with clozapine, a decades-old drug sometimes used to treat schizophrenia in people.
The researchers said that their finding suggested that such mice might provide scientists with a good model system for studying schizophrenia and testing new drugs designed to treat people suffering from it.
The latest study describes what happens to the mice when they lose the function of a brain protein called neuregulin, an important developmental protein that helps the brain form its distinct structures early in development and has been linked to schizophrenia and numerous other mental health problems.
The researchers found that when mice were deprived of neuregulin, their dendritic spines started to form, but did not mature completely - instead falling apart while the brain matures.
The effect of the loss was evident in behaviour tests, where mice display hallmarks of schizophrenia, such as social interaction problems and reduced anxiety.
The loss of the spines also led to the loss of the ability to adapt to and anticipate a startling noise - a classic sign of a schizophrenia-like state in mice.
This study provides support for a hypothesis about schizophrenia that implicates what are known as "glutamatergic" neurons.
Mueller says that it supports the hypothesis that glutamatergic neurons, which release the neurotransmitter glutamate, are also important in schizophrenia because the mice had problems with their glutamatergic synapses, which are located at dendritic spines.