Scientists identify mechanism that lowers impact of cocaine on the brain
For some, it is normal to show up inebriated or high on a drug most of the time. This is particularly true of cocaine addicts who abuse it to experience a short-term high, despite knowing the side effects of the drug, such as inability to take decisions and tendency to show compulsive craving and use.
A prolonged use of cocaine in excessive amounts may have long-term implications on both the body and the mind. But the situation becomes grave when a high dosage of cocaine causes brain cells to show cannibalistic behavior, that is, the tendency to eat away its own cells.
To mitigate the effect of cocaine on the brain, scientists from the Research Institute of the McGill University Health Centre (RI-MUHC) in Montreal discovered that microglia in the brain can help alleviate the impact of cocaine on the brain. In the study, titled “Microglial TNF-α Suppresses Cocaine-Induced Plasticity and Behavioral Sensitization” and published online in the journal Neuron in April 2016, the scientists showed how microglia can help decrease adverse effects to neural circuitry caused due to prolonged use of cocaine.
Commenting on the findings, Dr. David Stellwagen, a researcher from the Brain Repair and Integrative Neuroscience at the RI-MUHC and associate professor in the Department of Neurology and Neurosurgery at McGill University, said, “What we discovered is that cocaine activates these microglia, which causes the release of an inflammatory signal which then tries to reverse the changes that cocaine is inducing in the neurons.”
Beneficial impact of microglia may fade over time
The researchers used a mouse model to indicate how tumor necrosis factor (TNF) works on a specific set of synapses in the brain. Microglia play an important role in maintaining the normal brain functioning, and at the time of crisis, they release chemicals that influence the neurons to make adaptive changes to their connections; for example, it produces the inflammatory molecule TNF that can curb the synaptic changes caused by cocaine abuse.
On using a pharmaceutical agent that caused the production of TNF, the researchers found that the symptoms induced by cocaine use were reduced in the animals that were given this agent. Commenting on the reversal process made possible by microglia, Sarah Konefal, co-author and a McGill PhD student in the Integrated Program in Neuroscience in Dr. Stellwagen’s lab said, “These connections are really important for regulating the behavior response in animal models to drugs of abuse such as cocaine.”
However, the beneficial impact of microglia may diminish over time, according to the researchers. Thus, they stress on the need for developing treatment procedures that can help cut down relapse rates during the treatment for cocaine addiction.
Stellwagen said, “If we could develop a treatment that would suppress the craving that addicts have in stressful situations, or when they are re-exposed to situations in which they’d normally be taking the drug, that may allow them to avoid relapse. And that’s really the therapeutic goal of the work we have been doing.”
The findings of the study can play a pivotal role in finding alternative treatment options for recovery from cocaine or other addictive substances.
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