Researchers at New York University's Center for Neural Science and the Baylor College of Medicine have identified a protein that when removed from mice results in behaviors that are akin to those with autism and obsessive-compulsive disorders.
Their findings, which appear in the latest issue of the journal Neuron, may enhance our understanding of these and other neurological disorders.
The protein FKBP12, found in both humans and mice, is known to regulate mTOR, an enzyme involved in synaptic plasticity, or the ability of the neurons to change the collective strength of their connections with other neurons. Learning and memory are believed to result from changes in synaptic strength. mTOR also plays a role in behavioral plasticity - the ability to alter behavior in response to environmental changes.
The researchers eliminated FKBP12 from the brains of mice late in development and subsequently examined them for alterations in synaptic plasticity - specifically, in a brain area required for memory - and their behaviors. To test how different types of memory were affected by the absence of FKBP12, the NYU and Baylor scientists ran the mice through a variety of mazes and observed how they responded to certain objects.
The absence of the protein produced striking neurological and behavioral changes in the studied mice. Their results showed increased mTOR signaling, which regulates protein translation. This indicates that FKBP12 acts to limit mTOR activity. The researchers also found that the mice had enhanced synaptic plasticity and contextual memory, suggesting that FKBP12 negatively regulates these processes.