Addiction: Conflict Between Brain Circuits

This was the title of a lecture given today at the University of Texas Medical Branch (UTMB) in Galveston. I heard about on National Public Radio a few weeks ago, made a note to visit the Web site, registered and drove down from Houston to Galveston today to attend. In case you don't know why I have such a keen interest in the science of addiction, my November 10, 2009 post will explain it.

Dr. Nora Volkow, the speaker is the Director of the National Institute on Drug Abuse (NIDA), which is part of the National Institutes of Health (NIH). Quoting from her biography:

"Dr. Volkow's work has been instrumental in demonstrating that drug addiction is a disease of the human brain. As a research psychiatrist and scientist, Dr. Volkow pioneered the use of brain imaging to investigate the toxic effects of drugs and their addictive properties. Her studies have documented changes in the dopamine system affecting the actions of frontal brain regions involved with motivation, drive, and pleasure and the decline of brain dopamine function with age."

Of course, I couldn't resist taking some notes. This is just a sampling of all the interesting things that were said.

• After someone takes either food or amphetamines, you can see the same increase if dopamine in the nucleus accumbens. But drugs don't have the same satiating effects as food.
• Experiments can be conducted on humans using methylphenidate, which mimics the effects of cocaine. It also blocks the re-uptake of dopamine, causing the receptors to be flooded with the stuff. The "high" effect can be reported by the subject, and happens only if the substance is administered intravenously; if it is taken orally, it gets into the brain much more slowly and you see no effect at all, even allowing for a much longer period of time. So the dynamic aspect of drug administration is key.
• Different drugs have different clearance rates, and the "high" seems related to the rate of change of dopamine concentration, not to the absolute level. So if the level of dopamine goes up rapidly, then decays very slowly, the "high" does not persist, but starts dropping quickly as soon as the dopamine level has reached its maximum.
• Her imaging techniques allow her to study the effects of drugs on separate brain functions located in different places: the executive function (decision-making); inhibitory control (which allows a non-alcoholic to decide not to have one more drink, but is evidently damaged in the alcoholic); motivation and drive; memory and learning.
• Tests on animals who have been trained to push a lever to self-administer a drug have shown that causing the overexpression of dopamine D2 receptors causes the rats to lower their usage. As the substance injected to cause this overexpression wears off, over a period of 10 days or so, drug self-administration progressively returns to its previous level.
  
• Changes in dopamine receptors in the striatum correlate with changes in glucose metabolism in specific other parts of the brain, such as the orbital frontal cortex, which are also the effects observed in obsessive compulsive disorder (OCD). Another similarity between OCD and addiction is that when the reinforcement ceases (e.g., a lab rat is no longer given food when he is pressing the lever he had associated with this reward, or an addict no longer gets pleasure from his drug), he/it is still compulsively practicing the behavior.
• In the non-addicted brain, the ability to control actions is decreased by disruptions, such as anger, that affect the prefrontal cortex. That's why, when you just heard that your flight is canceled, you're more likely to go ahead and have that chocolate chip cookie that you had resisted earlier.