Released Today: New Insight into Root Cause of Auditory Hallucinations in Schizophrenia

Released Today: New Insight into Root Cause of Auditory Hallucinations in Schizophrenia

Posted: June 5, 2014

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A study by former NARSAD Young Investigator Grantee Stanislav S. Zakharenko, M.D., Ph.D., and his colleagues at St. Jude Children’s Research Hospital in Memphis, Tennessee, proposes that signaling errors in neurons originating in an area of the brain (the thalamus) that sends signals on to the auditory cortex for processing of sound might underlie auditory hallucinations in schizophrenia. The researchers used a mouse model of a developmental disorder closely linked to schizophrenia to try to identify the molecules and brain circuits that might underlie hallucinations.

The absence, or deletion, of a small piece of chromosome 22 is known to cause a developmental disorder—22q11.2 deletion syndrome—that is characterized by heart and palate abnormalities, intellectual disability, and a wide range of other abnormalities. This deletion syndrome also carries a high risk for developing schizophrenia; for this reason researchers often study the deletion syndrome as a genetic model of the illness.

This new study, published online June 6th in Science, reports that a mouse model of 22q11.2 deletion syndrome contained signaling deficits in neurons that connect the thalamus—the “relay station” of the brain that sends information from sensory systems to the parts of the cortex that interprets the signals—to the auditory cortex, where sounds are decoded. These decreased signals were specific to cells originating from the thalamus; they were not found in other neurons in the auditory cortex.

The researchers observed these signaling problems while measuring the electrical activity of neurons in brain slices obtained from the 22q11.2 deletion mouse model. Bathing the slices in antipsychotic medications reversed the deficits. The researchers report that this may offer new insight into how antipsychotic medications effectively treat auditory hallucinations—by correcting the malfunction of these neurons originating in the thalamus—and may offer a new target of neuronal malfunction underlying schizophrenia-associated psychosis.

The research is "a significant advance" in studying 22q11 deletion syndrome, said Columbia University researcher and two-time NARSAD Grantee Christoph Kellendonk, Ph.D., who was not involved in the study. But he cautioned against drawing conclusions about schizophrenia from the data. No direct cause-and-effect link between the signaling abnormalities and auditory hallucinations has yet been made. Further studies will be required to learn more.

Read more about this research on the Schizophrenia Research Forum.

Read the abstract for this research.