One of NIDA’s goals is to try to understand the individual differences that contribute to whether or not someone who takes a drug will become addicted to it. Dr. Rutter’s research focuses on three types of differences: Environmental, developmental, and genetic and epigenetic.
Methamphetamine alters brain structures involved in decision-making and impairs the ability to suppress habitual behaviors that have become useless or counterproductive. The two effects were correlated, indicating that the structural change underlies the decline in mental flexibility.
Ketoprofen, an anti-inflammatory agent commonly prescribed to treat arthritis, reduces neuronal damage in rats that have been exposed to chronic stress and methamphetamine. If this finding of a recent NIDA-supported study extrapolates to humans, anti-inflammatory medications may gain a place in the treatment of methamphetamine addiction.
Researchers have shut down laboratory rats’ compulsive cocaine seeking by stimulating an area of the animals’ prefrontal cortex. The finding raises the possibility that stimulating neurons in this brain area may weaken or break cocaine’s grip on the behavior of people who are addicted to the drug.
A meta-analysis of 13 genome-wide association studies of African Americans’ smoking patterns confirms the significance of genetic variation in region 15q25.1. The analysis also tentatively implicates several genome locations that have not previously been associated with smoking behaviors.
Dr. Marilyn Huestis of NIDA’s Intramural Research Program talks about conducting research on drug effects with human subjects, developing tests to help law enforcement identify drugged drivers, and an assay to help identify children whose prenatal exposure to anti-HIV drugs may put them at risk for adverse developmental outcomes.
New research demonstrated that, in rhesus monkeys, ongoing cocaine exposure weakens two brain functions that people require for successful behavioral change: cognitive flexibility and memory. But the study determined that these changes may not be permanent.
Clinical trials of N-acetylcysteine to help people recovering from drug abuse avoid relapse have demonstrated only moderate efficacy. New NIDA-supported research shows that while a low dose of the medication activates receptors associated with lowered drug-seeking behavior, a higher dose appears to activate receptors associated with increased drug-seeking behavior. The result suggests that a medication or combination of medications that stimulate the receptor GluR2/3 and block mGluR5 may work better than N-acetylcysteine alone.