What Is Reuptake?

Understanding Fibromyalgia and ME/CFS Drugs

Neruotransmitters help messages brige the gaps between brain cells. KTSDESIGN/Getty Images

When you're learning about treatment options for fibromyalgia and chronic fatigue syndrome, you're likely to come across the term "reuptake inhibitors." It describes a type of antidepressant that we're commonly prescribed, including the FDA-approved fibromyalgia medications Cymbalta (duloxetine) and Savella (milnacipran).

But do you understand what reuptake means? When I first started learning about reuptake inhibitors, I was confused -- I knew that these conditions were believed to involve low levels of the brain chemicals serotonin and norepinephrine, so I didn't get why we'd want to inhibit something that involved them.

It was a long time before I finally found an explanation that made sense, but it involved complex medical terminology that I only understood because I'd been researching them for years. Here, I try to break it down into language that's easier to grasp.

What Is Reuptake?

First, a little bit about how your brain works:

Your brain cells (neurons) are separated by little gaps. When your brain transmits messages from one neuron to another, it bridges those gaps by releasing specialized chemicals called neurotransmitters.

After a while, the space between the cells basically gets cluttered up with a lot of used neurotransmitters. It's kind of like opening your mail and ending up with a pile of empty envelopes -- the envelopes were important for getting the mail to you, but you no longer need them. Your brain cleans up the mess by reabsorbing (reuptaking) the neurotransmitters so they can be recycled.

Now let's simplify it and go a step further:

Imagine a spider perched on the back of a chair. He wants to get to the table. so he starts shooting a strand of web across the gap. It shouldn't be a problem, but an oscillating fan across the room keeps turning that direction and blowing the web away before the spider can complete the journey.

Now, imagine that someone changes the speed on the fan so that it oscillates more slowly. That gives the spider enough time to cross the gap before the web is blown away.

The spider is the message, the web is the neurotransmitter, and the fan is reuptake. When you slow reuptake, the message has enough neurotransmitter to get where it's going. Reuptake inhibitors don't increase the total amount of neurotransmitter in your brain, but they do increase the amount of time it's available. That helps messages get where they're going.

How Reuptake Applies to Us

Researchers theorize that the brains of people with fibromyalgia, chronic fatigue syndrome, and many other neurological illnesses have low levels of certain neurotransmitters or don't use their neurotransmitters properly. That's called neurotransmitter dysregulation, and it's believed to be responsible for many of our symptoms, including brain fog and pain amplification.

Research shows that slowing reuptake helps alleviate symptoms in a significant number of people with these illnesses.

Older reuptake inhibitors slowed the process for all neurotransmitters, which led to a lot of unwanted effects. Modern reuptake inhibitors selectively target specific neurotransmitters -- especially serotonin and norepinephrine. They're called:

  • Selective serotonin reuptake inhibitors (SSRIs)
  • Serotonin-norepinephrine reuptake inhibitors (SNRIs)

While these drugs cause fewer problems than the older medications, they still have a long list of side effects. Part of the problem is that we don't have neurotransmitter deficiencies in every area of the brain, so the medication may improve transmission in one area while disrupting it in another.

However, a new type of SSRI is emerging that may provide relief with fewer side effects by targeting the brain cell that receives a neurotransmitter's message. That cell is called a receptor, and each receptor is designed to only receive messages sent by certain neurotransmitters. Essentially, the receptor is locked. Only the right chemical keys can open it.

This new drug targets certain serotonin receptors with simulated keys and tricks them into opening, making it easier for messages to flow from cell to cell. At least one drug of this type -- Viibryd (vilazodone) -- is currently approved for depression in the United States. (However, iIt has not been researched for either fibromyalgia or chronic fatigue syndrome.)

Learn more about how these drugs work for our conditions:

To see the symptoms linked to neurotransmitter deficiencies, along with treatment options, read:

Sources:

Fields, R. Douglas, Ph.D. (2009) The Other Brain. New York: Simon & Schuster.

Goldstein, J. Alasbimn Journal2(7): April 2000. AJ07-5. "The Pathophysiology and Treatment of Chronic Fatigue Syndrome and Other Neurosomatic Disorders: Cognitive Therapy in a Pill."

Smith AK, et al. Psychoneuroendocrinology. 2008 Feb;33(2):188-97. "Genetic evaluation of the serotonergic system in chronic fatigue syndrome."

2008 University of Maryland Medical Center. All rights reserved. "Chronic Fatigue Syndrome"

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