Thursday, 7 April 2016

The GABA Transmitter: A Top Pain Reducer

Today's post from (see link below) is another example of how can take an enormously complex subject and explain it in terms that the ordinary person can understand. Having said that, this post is another in the long line of 'we've discovered this but you'll have to wait years for any practical results' research findings. However, that doesn't mean it shouldn't be reported, especially to long-suffering neuropathy patients. In that way, we learn to understand the workings of our nervous system bit by bit until we can eventually tell our doctors a thing or two. This article concerns the chemical GABA transmitter from the brain, which is responsible for dimming nerve pain signals. If you hit your finger and then rub it better, the pain often diminishes - this is the GABA transmitter at work. However, with chronic pain, which is daily and unrelenting, the GABA transmitters become elasticised with all the work they have to do, and work less well in reducing the sensation of pain. The aim is to reverse this elasticity and maintain the ability to reduce pain signals. Simple eh! No of course not, but this article tries to make it as simple as possible. Worth a read.

Potential new source for pain inhibition found Date:April 4, 2016 Source:University of Texas at Dallas 

Findings offer potential new therapeutic direction to investigate

A UT Dallas scientist has found a new neurological mechanism that appears to contribute to a reduction in pain.

According to Dr. Ted Price, associate professor in the School of Behavioral and Brain Sciences, the discovery of neuroligin-2 as a cause exacerbating chronic pain is significant for the research community. Although the findings likely won't immediately lead to new pain therapies, the findings offer a potential new therapeutic direction to investigate, he said.

Price's research on the topic has recently been published online in Pain, the journal of the International Association for the Study of Pain.

The study focused on the body's inhibitory networks -- a series of biochemical reactions that decrease certain neurological activity, such as pain. Price said a great deal of previous research in this area has focused on the activity of the neurotransmitter GABA, a chemical released by nerve cells in the brain.

Normally a GABA neurotransmitter acts to inhibit neuronal activity, such as pain. However, when pain becomes chronic there is strong evidence that a process called GABAergic plasticity can cause GABA to lose its inhibitory activity, sometimes making the pain even worse.

The source of these excitatory actions in neuronal circuits has been broadly attributed to chloride ions, but Price's research has found another potential cause of GABAergic plasticity: synaptic adhesion molecules called neuroligin-2.

"From a basic science perspective, we're really excited about it because it demonstrates that the types of GABAergic plasticity that can occur in the setting of chronic pain are more diverse than we've appreciated before," he said.

Price, who heads the undergraduate research program in neuroscience in the School of Behavioral and Brain Sciences, focuses much of his research on understanding the neuroscience behind pain, particularly chronic pain. He said individuals with chronic pain typically don't receive the pain-reduction benefits delivered by inhibitory systems. Instead, they often experience increased pain.

"When you hit your hand with a hammer, almost everybody has the same reflex reaction -- that is, to rub your finger which, in turn, helps to reduce pain. The reason that works is because it increases GABAergic inhibition in the spinal cord," Price said. "However, people who have chronic pain -- if they do the same thing -- find that rubbing it actually makes the pain worse. That's because the GABAergic system loses its efficacy and, in fact, can become excitatory."

Price said the current research is another step in determining why the GABAergic system stops working correctly in some people; it provides a second theory for what drives the system.

"Having two ideas and different models will allow us to determine what the therapeutic opportunities are -- creating something that will change that back to normal. The lack of performance in the inhibitory system is very detrimental to those who are in chronic pain," he said.

Price said the development of chronic pain is, in essence, one's body "learning" something that is bad.

"It's changing the way the body functions -- it's learning. That learning, in the case of chronic pain, is aberrant -- it's causing the situation to get worse. If we can figure out what that form of learning was, then we can potentially reverse it. Understanding that the GABAergic system changes during this form of learning potentially offers a new therapeutic avenue," he said.

Story Source:

The above post is reprinted from materials provided by University of Texas at Dallas. Note: Materials may be edited for content and length.

Journal Reference:
Ji-Young V Kim, Salim Megat, Jamie K Moy, Marina N Asiedu, Galo L Mejia, Josef Vagner, Theodore J Price. Neuroligin-2 regulates spinal GABAergic plasticity in hyperalgesic priming, a model of the transition from acute to chronic pain. PAIN, 2016; 1 DOI: 10.1097/j.pain.0000000000000513

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