From the NYT sensational article on ADD ADHD
This is the thing that startled me:
Psychostimulants like Adderall and Ritalin help by blocking the transport of dopamine back into neurons, thus increasing its level in the brain.
I’d understood that the stimulants work by increasing the release of dopamine and norepinephrine.
When I looked this up on the net, I found studies supporting both effects, including contradictory studies from Dr. Volkow.
What’s a poor boy to do? I’m sure, or at least hopeful, that some of you out there can clear this up?
Dr. Nora D. Volkow, a scientist who directs the National Institute on Drug Abuse, has studied the dopamine reward pathway in people with A.D.H.D. Using a PET scan, she and her colleagues compared the number of dopamine receptors in this brain region in a group of unmedicated adults with A.D.H.D. with a group of healthy controls. What she found was striking. The adults with A.D.H.D. had significantly fewer D2 and D3 receptors (two specific subtypes of dopamine receptors) in their reward circuits than did healthy controls. Furthermore, the lower the level of dopamine receptors was, the greater the subjects’ symptoms of inattention.
Yes, we are little different aren’t we?
If you don’t want to wade through these, I’ll summarize them in another post.
Aaron T. Mattfeld, a neuroscientist at the Massachusetts Institute of Technology, now at Florida International University in Miami, compared the brain function with resting-state M.R.I.s of three groups of adults: those whose childhood A.D.H.D persisted into adulthood; those whose had remitted; and a control group who never had a diagnosis of it. Normally, when someone is unfocused and at rest, there is synchrony of activity in brain regions known as the default mode network, which is typically more active during rest than during performance of a task. (In contrast, these brain regions in people with A.D.H.D. appear functionally disconnected from each other.) Dr. Mattfeld found that adults who had had A.D.H.D as children but no longer had it as adults had a restoration of the normal synchrony pattern, so their brains looked just like those of people who had never had it.
But from MIT
In people without it, when the default mode network is active, another network, called the task-positive network, is inhibited. When the brain is focusing, the task-positive network takes over and quiets the default mode network. This reciprocal relationship is necessary in order to focus.
Both groups of adult A.D.H.D. patients, including those who had recovered, displayed simultaneous activation of both networks, as if the two regions were out of step, working at cross-purposes. Thus, adults who lost most of their symptoms did not have entirely normal brain activity.
So, if we lose most of our symptoms, like in a perfect work or school environment, our brains still function differently.
The NYT article – What?? You haven’t read it yet?!
It’s two sides of the same coin. Our brains don’t effectively produce or utilize certain neurochemicals like dopamine. In order to use dopamine, it has to be released from inside the neuron, where it’s produced, out into the neural pathway. But because our neurons aren’t producing adequate levels of dopamine, they just don’t want to let it go. Medications that encourage the neurons to let go of the dopamine are release facilitators. Once the dopamine does get out into the pathway, our greedy little neurons are quick to suck it back in and hold onto it again. Stimulant medication keeps the neurons from sucking the dopamine back in. That “sucking back in” is called reuptake, so the medication is a reuptake inhibitor.
For a really good, basic lesson on how this works, I recommend Khan Academy’s videos on the neuron and nervous system. Brain chemistry and dopamine release made so much more sense after I watched the series. https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/v/anatomy-of-a-neuron
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Hee hee! I just realized you’re a doctor and you already know all that. Hopefully it’s helpful to other non-docs like me. Khan Academy may be a bit remedial for you, but the videos really did make it all fall into place. It’s important for all of us to understand what we’re actually doing when we take medication. I can’t tell you how many times I’ve heard someone say that doctors don’t really know what the medication does in the brain, just that it seems to work. I think it’s more accurate to say that most of us don’t understand what our doctors tell us the medication does in the brain, just that it seems to work. Once it works, it’s easier to understand the explanations of why it works.
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heather – well, I think it’s complicated, and I think we kind of know and kind of don’t know, both at the same time. Some of the medications are reuptake blockers, and some are release stimulators, and some are both, and right now I’m quite unclear about which is which.
for the moment I’m going to take Dr. Mason’s word – “methylphenidate (ritalin) is only a reuptake inhibitor and that amphetamine (adderall) is both a reuptake inhibitor and a release-facilitator.”
thank you for the comment and for the link
Heather – that’s a good reference. Thanks. Doug
Doug, I think the simple explanation is that methylphenidate is only a reuptake inhibitor and that amphetamine is both a reuptake inhibitor and a release-facilitator. If a person is as naturally undersupplied with dopamine as you and I seem to be, ANYTHING that raises function in the dopamine-starved circuits is welcome. Any more complicated than that, though, and I’m on the sidelines. Lol! Oren
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oren -thanks. i seem to have been misinformed- again!