MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Altered energy balance has been studied in drug abuse but the fundamental source of energy, mitochondria, has not been well examined. In this study we found that a molecular regulator of mitochondrial fission (division) is increased in the nucleus accumbens, a major brain reward region, of rodents exposed to repeated cocaine and postmortem samples of cocaine dependent individuals. We further found that mitochondrial fission is increased in a nucleus accumbens neuron subtype in rodents that self-administer cocaine. Pharmacological blockade of mitochondrial fission can prevent physiological responses to cocaine in this neuron subtype while reducing cocaine-mediated behaviors. Finally, genetic reduction of mitochondrial fission in this neuron subtype in the nucleus accumbens can reduce drug (cocaine) seeking in rodents previously exposed to cocaine. In contrast, increasing mitochondrial fission, in this neuron subtype, enhances cocaine seeking behavior.
MedicalResearch.com: What should readers take away from your report?
Response: Mitochondria, in a specific neuron subtype within the nucleus accumbens, play a role in drug (cocaine) seeking in rodents that were previously exposed to cocaine.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Response: It will be important to understand the exact role the mitochondria have in these neurons when animals are exposed to cocaine. We have some insight into the physiological mechanisms but further work is needed to understand how the mitochondria are altering this process. It will also be important to determine if these mitochondrial changes occur with other drugs of abuse, such as opiates.
MedicalResearch.com: Is there anything else you would like to add?
Response: Overall it is important to not only understand molecular mechanisms of drug abuse but to identify the neuron subtypes in which these altered mechanisms occur. This will allow us to pinpoint the neurobiological changes occurring in vulnerable neuron subtypes in addictive disorders. In this study we identified a new molecular mechanism, that leads to altered mitochondrial changes, in a specific neuron subtype of the nucleus accumbens after repeated exposure to cocaine.
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Ramesh Chandra, Michel Engeln, Christopher Schiefer, Mary H. Patton, Jennifer A. Martin, Craig T. Werner, Lace M. Riggs, T. Chase Francis, Madeleine McGlincy, Brianna Evans, Hyungwoo Nam, Shweta Das, Kasey Girven, Prasad Konkalmatt, Amy M. Gancarz, Sam A. Golden, Sergio D. Iñiguez, Scott J. Russo, Gustavo Turecki, Brian N. Mathur, Meaghan Creed, David M. Dietz, Mary Kay Lobo. Drp1 Mitochondrial Fission in D1 Neurons Mediates Behavioral and Cellular Plasticity during Early Cocaine Abstinence. Neuron, 2017; 96 (6): 1327 DOI: 10.1016/j.neuron.2017.11.037
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