The gene involved is one of several that has been linked to the overall development of autism and is a gene vital for normal brain development. The research published in the neuroscience journal Neuron specifies that this gene plays a vital role in addiction associated behaviors.
“In our lab, we investigate the brain mechanisms behind drug addiction — a common and devastating disease with limited treatment options,” said Christopher Cowan, PhD, director of the Integrated Neurobiology Laboratory at McLean and an associate professor of Psychiatry at Harvard Medical School. “Chronic exposure to drugs of abuse causes changes in the brain that could underlie the transition from casual drug use to addiction. By discovering the brain molecules that control the development of drug addiction, we hope to identify new treatment approaches.”
The study conclusively linked the fragile X mental retardation protein, or FMRP, the leading single gene cause of autism and disability to addiction as cocaine uses FMRP to facilitate brain changes involved in addiction-related behaviors.
“We know that experiences are able to modify the brain in important ways. Some of these brain changes help us, by allowing us to learn and remember. Other changes are harmful, such as those that occur in individuals struggling with drug abuse,” said Cowan and Smith. “While FMRP allows individuals to learn and remember things in their environment properly, it also controls how the brain responds to cocaine and ends up strengthening drug behaviors. By better understanding FMRP’s role in this process, we may someday be able to suggest effective therapeutic options to prevent or reverse these changes.”
Laura N. Smith, Jakub P. Jedynak, Miles R. Fontenot, Carly F. Hale, Karen C. Dietz, Makoto Taniguchi, Feba S. Thomas, Benjamin C. Zirlin, Shari G. Birnbaum, Kimberly M. Huber, Mark J. Thomas, Christopher W. Cowan. Fragile X Mental Retardation Protein Regulates Synaptic and Behavioral Plasticity to Repeated Cocaine Administration. Neuron, 2014; 82 (3): 645 DOI: 10.1016/j.neuron.2014.03.028