How Stimulants Control Hyperactivity


I recently stumbled on this article that talks about stimulant medications and how they reduce hyperactivity — a phenomenon which seems at first glance to be quite paradoxical. The dopamine receptors called DRD4 located in the basal ganglia and neighboring brain regions are responsible for this effect; in rat studies, DRD4 knockout rats (rats genetically modified so they have fewer to no DRD4 receptors in these areas) exhibited greatly increased motor activity (i.e. the fidgeting and bouncing off the walls I’m sure so many of you are familiar with!). When these rats were treated with amphetamine, their excess motor activity (hyperactivity) disappeared. There’s more to it, naturally, but that’s the crash course.

This intrigued me for two reasons:

One, because this means that hyperactivity is probably inherited genetically, for the most part, and perhaps is somewhat independent from other aspects of ADHD (inattention, impulsivity, etc). This could lead to more refined subcategories of ADHD, and hopefully to more individualized pharmacotherapy if Big Pharma ever gets around to updating their hopelessly antiquated stimulant formulations (this shit’s been around since 1937, we’re ready for version 2.0).

Two, because this suggests that ADHD arises from dysfunctional DRD4 receptors in SUBcortical areas (lizard brain areas) rather than in the prefrontal cortex (associated with planning, working memory, impulse control, sustained attention, etc). Non-stimulant medications such as Strattera and Intuniv primarily target the prefrontal cortex and exhibit little to no effects in the subcortical areas, whereas stimulants target both the PFC and aforementioned “lizard brain parts” — and as we all know, stimulant medications are far more effective than any other available treatment.

Moral of the story: the ADHD kid’s lizard brain is tragically messed up, and apparently we all need a properly functioning lizard in our brains in order to sit still and be boring. Damn lizards.

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