Researchers map dopamine based chronic-pain pathway in the spinal cord and brain.


A chemical in the brain typically associated with cognition, movement and reward-motivation behaviour, among others, may also play a role in promoting chronic pain, according to new research from researchers at The University of Texas, University of Arizona and the University of Alabama.  The chemical, dopamine, sets the stage for many important brain functions, but the mechanisms that cause it to contribute to chronic pain are less well understood.

In a recent paper published in The Journal of Neuroscience, the researchers followed the sequence of pain impulses traveling from the brain to the spinal cord in mice. They found that by removing a collection of neurons called A11 that contain dopamine, chronic pain was selectively diminished.  The data findings demonstrated a novel role for how dopamine contributes to maintaining chronic pain states.

The team hypothesize that this may open up new opportunities to target medicines that could reverse chronic pain.  They go on to explain that pain signals travel like electricity from an injury to the spinal cord where they pass on electrical or chemical pain signals to other cells. Those pain signals then travel upward and relay that information to neurons in the brain where they can be distributed throughout. There is no single pain center in the brain, but there is substantial evidence that chronic pain changes how these pain centers are activated.

In people with chronic pain, neurons continue to send pain signals to the brain, even in the absence of injury, but the causes of this are not known, the researchers explain. A potential explanation comes from A11. In the current study these neurons didn’t affect acute pain, but they did have a profound effect on chronic pain. By targeting these neurons in mice with chronic pain, the researchers permanently reversed a chronic pain state.

Previous studies have examined the role of other neurotransmitters in chronic pain including norepinephrine and serotonin.  By process of elimination the team decided to look more closely at dopamine. The researchers used a toxin that affected A11 neurons, and that’s when they found that acute pain signals were still normal, but chronic pain was absent.

In 2011, the Institute of Medicine estimated that more than 100 million Americans suffer from chronic pain, a condition that costs more than $600 billion each year in medical care and lost productivity.

The team surmise that understanding the basis of chronic pain and all of its contributing factors could help point to more effective treatments.  In future studies, the researchers state that they would like to gain a better understanding of how stress interacts with A11 and how the interaction between molecular mechanisms promote chronic pain and dopamine.

Source:  The University of Texas at Dallas 

 

Descending dopaminergic fibres within the spinal cord originate in the A11. (A) Dopamine acts on all five dopamine receptors that are distributed non-uniformly through the dorsal and ventral horns of the spinal cord (Adapted with permission from Zhu et al., 2007). Descending noradrenergic fibres originating in the A5, A6 and A7 nuclei of the pons innervate the spinal cord. Schematic adapted with permission from Björklund and Dunnett (2007).  Dopamine: a parallel pathway for the modulation of spinal locomotor networks.  Whelan et al 2014.

Descending dopaminergic fibres within the spinal cord originate in the A11. (A) Dopamine acts on all five dopamine receptors that are distributed non-uniformly through the dorsal and ventral horns of the spinal cord (Adapted with permission from Zhu et al., 2007). Descending noradrenergic fibres originating in the A5, A6 and A7 nuclei of the pons innervate the spinal cord. Schematic adapted with permission from Björklund and Dunnett (2007). Dopamine: a parallel pathway for the modulation of spinal locomotor networks. Whelan et al 2014.

 

 

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s