Where does addiction begin? Where does chemical dependence take over the simple urge to use? When does the addiction take over the reward centers in the brain? When does hunting for the “high” end and the fear of the “come-down” begin? Here we discuss the addiction switch and how it explains it all–or at least tries to.
Many research has been about about addiction, and perhaps one of the most significant study made is on the so-called “addiction switch.”
According to studies, addiction can be best described as a process of turning on a neurochemical switch. Here, repeated drug use forces key areas in the brain to undergo somewhat of a permanent, if not long-term, change. Part of this addiction switch are the areas connecting the cortex to the striatum, the part responsible for our feelings of motivation, movement, and the formation of habits.
In an April 10, 2008 issue of Neuron, researchers Nigel Bamford, a pediatric neurologist at the University of Washington in Seattle, used innovative imaging techniques to probe and document the harvested still-living brains of mice. In this study, the mice have been given methamphetamine for a span of 10 days before it was withdrawn. It showed that the doses of meth given repeatedly to the mice caused their corticostriatal circuits to be depressed, therefore undermining the complex systems that normally govern them.
Normally, the midbrain, which is responsible for the release of dopamine, becomes active when the brain receives an unexpected stimuli. The dopamine molecules released bind to the feedback receptors of the cortex, silencing the cortical terminals that have been previously inactive. This filters out any activity that isn’t related to the new stimulus so that the brain can focus on the present situation. When psychoactive drugs such as meth and cocaine are presented to the brain, the brain takes on a new state, in which it works only when the drug is presented.
With the mice, the chronic surges of drug-induced dopamine adversely affect the feedback sensors of the interneurons, dialing down the activity and keeping them down even after the dopamine surge have subsided. This results in reduced stimulation of the corticostriatal circuits, keeping the cortex depressed.
In other words, the 10 days of drug use in mice have shut down the corticostriatal system’s normal function, and only when drugs is introduced in the mice can the cortical terminals be “renormalized” again, but only until the effects of the drugs last. When the drugs wear off, the system shuts down again, only to seek drugs, on which it is now dependent on. For mice, this dependence can last for 140 days after the withdrawal, which can be decades for humans.
This research has paved the way for more studies that sheds light for potential addiction therapies.
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