It’s no secret that cocaine is a highly addictive drug. Until recently, though, the mechanisms behind its ability to alter and control the brain as an addictive substance have not been known.
A new study conducted by researchers at Mount Sinai School of Medicine has uncovered the process for how cocaine corrupts the brain, and researchers believe the information will provide key insights into the development of new therapies to treat cocaine addiction.
Mary Kay Lobo, Ph.D., postdoctoral fellow in the department of neuroscience and lead author of the study said that the findings are the first to connect the activation of specific neurons to a capacity for altering cocaine reward.
In previous studies, cocaine has been linked to the reward circuits in the brain.
Sniffing cocaine causes high levels of dopamine secretion to occur in a central region of the brain. Dopamine plays a crucial role in the brain’s response to reward as well as in its response to addictive drugs.
In the new study, researchers discovered that two main neurons (D1 and D2) found in the nucleus accumbens region of the brain exert opposing effects on cocaine reward. The nucleus accumbens region is a critical area of the brain’s reward center.
By using optogenetics technology, researchers found that activation of the D1 neurons increases cocaine reward while activation of D2 neurons decreases reward. Optogenetics provides a method to optically control neuron activity in rodents that move about freely.
“The data suggest a model whereby chronic exposure to cocaine results in an imbalance in activity in the two nucleus accumbens neurons: increased activity in D1 neurons combined with decreased activity in D2 neurons,” Lobo. “This further suggests that BDNF-TrkB signaling in D2 neurons mediates this decreased activity in D2 neurons.”
Opposite cocaine reward similar to those found when activating each neuron is achieved by disrupting brain-derived neurotrophic factor, which is a protein in the brain known for its involvement in neuronal survival, learning, and memory and drug abuse signaling through its receptor TrkB in D1 or D2 neurons.
Eric Nestler, M.D., PH.D., a co-author of the study, said that the information provides new insight into the process of how cocaine affects two neuronal subtypes differently that are heterogeneously intermixed in the nucleus accumbens.
“We can use this information to potentially develop new therapies for cocaine addiction, possibly aimed at altering neuronal activity selectively in either neuronal subtype,” he added.
The findings of this study were published in the Oct. 15, 2010 edition of Science.
According to the 2008 National Survey on Drug Use and Health, approximately 36.8 million Americans aged 12 and older had tried cocaine at least once in their lifetime.