For years, scientists have known that mitochondria in brain cells play a role in brain disorders such as depression, bipolar disorder, anxiety and stress responses. But recently, scientists have identified significant mitochondrial changes that take place in cocaine addiction, and they have been able to block them.

Mitochondria serve as the power source of cells, and they play an important role in the way cells function in the body.

In mice exposed repeatedly to cocaine, researchers identified an increase in a molecule that plays a role in mitochondria division (or fission) in a reward region of the brain. Authors demonstrate an increase of dynamin-related protein-1 (Drp1), the mitochondrial fission mediator, in nucleus accumbens (NAc) after repeated cocaine exposure and in cocaine-dependent individuals.

Mdivi-1, a demonstrated fission inhibitor, blunts cocaine seeking and locomotor sensitization, while blocking c-Fos induction and excitatory input onto dopamine receptor-1 (D1) containing NAc medium spiny neurons (MSNs).

Drp1 and fission promoting Drp1 are increased in D1-MSNs, consistent with increased smaller mitochondria in D1-MSN dendrites after repeated cocaine. Knockdown of Drp1 in D1-MSNs blocks drug seeking after cocaine self-administration, while enhancing the fission promoting Drp1 enhances seeking after long-term abstinence from cocaine according to research published in Neuron.

"We are actually showing a new role for mitochondria in cocaine-induced behavior, and it's important for us to further investigate that role," said the senior author.

The researchers initially studied the mitochondria in cocaine-exposed mice and determined that mitochondria fission increased in the major reward region of the brain. To confirm this same change in humans, researchers were able to identify similar changes in the mitochondrial fission molecule in tissue collected from post mortem individuals who were cocaine dependents.

Senior author said that this latest research could help researchers better understand changes in brain cells and mitochondria from other addictive disorders.

http://www.cell.com/neuron/abstract/S0896-6273(17)31090-5