A branch of the National Institutes of Health, the National Institutes of Drug Abuse (NIDA), funded a study discovering neuronal circuitry in a rodent brain that controls anhedonia caused by pain. Anhedonia is a lowered motivation to participate in behavior that is driven by rewards. The researchers involved in the study were successful in changing the circuitry and increasing motivation levels.
Components of pain
Pain has two components, that is, the pain felt (sensory) and the emotional reaction to pain (affective). The affective component leads to anhedonia which can be a symptom of depression. Anhedonia also raises a person’s susceptibility to opioid use disorder (OUD). The relationship between drug abuse and the affective part of pain explains NIDU’s interest in the subject.
According to Nora D. Volkow, M.D, the NIDA Director, chronic pain is not just a physical phenomenon as the study shows that affective pain is also biological. Their results could lead to treatment options that look into the emotional and motivational impact of pain.
Researchers from Washington University in St. Lois looked into other studies that showed how rats in pain were likely to take more heroin. At the same time, their motivation for rewards like sugar tablets lowered.
The team wanted to identify the circuitry involved in this kind of behavior. The circuitry would enable the researchers to correlate pain with a decrease in motivation. They evaluated dopamine neuron activity in the ventral tegmental area. This area of the brain initiates rewarded behavior. Neuronal activity was measured when they pressed a lever to earn a sugar tablet.
How researchers conducted the study
The researchers wanted to study the effect of pain on the activity of dopamine neurons. Therefore they split the mice into two groups. They injected the first group in the hind paw with a substance that would cause inflammation, while they used saline with the control group.
Within 48 hours, the team noticed that rats in pain would press the levers less. They also had lower activity in their dopamine neurons. Researchers noticed that the pain activated the rostromedial tegmental nucleus, which makes GABA which in turn inhibits dopamine neurons.
Fortunately, they were able to reverse the process and restore activity.
