Coupling of brain proteins may prompt new treatments for schizophrenia, addiction

Researchers at the University of Toronto, the Centre for Addiction and Mental Health (CAMH) and the Hospital for Sick Children (HSC) have discovered a cellular communication method in the brain that could lead to improved treatments for schizophrenia and addiction.

Many of the symptoms associated with schizophrenia and addiction are caused by either too much or too little dopamine and GABA, chemicals in the brain that help regulate learning, memory, emotion and cognition. In a study published in the Jan. 20 edition of the journal Nature, researchers demonstrate how proteins can modify each other's function - including the ability of neurons to accept or reject dopamine and other neurochemicals - by binding to each other.

"What we found is a previously unknown method of signal transduction between two structurally different neurotransmitter receptor systems, that is, the direct physical coupling of these proteins," says senior author Dr. Hyman Niznik, associate professor of psychiatry and pharmacology at U of T and section head, laboratory and molecular neurobiology at CAMH. "This may provide us with a new therapeutic window on how to restore normal cellular function in diseases like schizophrenia with the right medication that can either block this interaction or make it happen." Brain cells communicate with each other via neurotransmitters - natural chemicals that interact with proteins, or receptors, on adjacent neurons. There are many different types of receptors in the brain, some of which respond only to dopamine and some only to the neurotransmitter GABA [g-aminobutyric acid]. Of the many dopamine receptors, two - D1 and D5 - are very similar and respond to the same drugs. Many of the negative symptoms of schizophrenia and addiction are regulated by D1-like receptors.

Niznik and his team of researchers demonstrated that dopamine D5 receptors can directly modify the function of GABA receptors by directly binding to them and forming

Contact: Megan Easton
University of Toronto

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