Researchers at Mount Sinai School of Medicine have rejected the popular belief that both morphine and cocaine act similarly and said that they produce opposite effects on the brain.
They found that a protein called brain-derived neurotrophic factor (BDNF), which is increased in cocaine addiction, is inhibited in opioid addiction.
"Our study shows that BDNF responds completely differently with opioid administration compared to cocaine," said Ja Wook Koo, PhD, Postdoctoral Fellow in the Department of Neuroscience at Mount Sinai School of Medicine.
"Morphine creates reward by inhibiting BDNF, whereas cocaine acts by enhancing BDNF activity."
BDNF is key to several functions in the brain and peripheral nervous system, notably for making new nerve cells and helping the survival of existing ones. It is also known to activate reward centers in the brain.
Cocaine causes an increase in the presence of BDNF in a reward center of the brain called the nucleus accumbens, which results in activation of the reward center.
In the current study, the research team found that morphine suppresses BDNF in a different reward center of the brain known as the ventral tegmental area (VTA), in order to achieve reward and chronic addiction.
The morphine caused a depletion of BDNF in the VTA of mice, which activated the reward centers. However, when BDNF was administered to the VTA of mice, it inhibited that reward. When BDNF was administered to the nucleus accumbens, there was no reward.
When researchers analyzed morphine-induced changes in gene expression in the nucleus accumbens, the area of the brain in which morphine caused no reward or response they found that two genes, sox11 and gadd45g, mediated the brain's response to morphine, preventing any reward and addiction.
The study was recently published in the journal Science.