A study presented at the Ninth Annual Canadian Neuroscience Meeting suggests that a biological basis for the link between anxiety and chronic pain may have been found.

Min Zhuo, PhD, the study’s presenter, and his team note also that a molecule that may help reduce chronic pain-related anxiety may have been identified.

Chronic pain can be viewed as a learned memory, and persistent pain can become chronic because neurons can become more efficient at transmitting pain signals. This is defined as Long Term Potentiation, or LTP, explains a news release from the Canadian Association for Neuroscience.

Previous studies on animal models in Zhuo’s lab at the University of Toronto suggest, per the release, that LTP occurs in the anterior cingulate cortex (ACC), and that inhibiting LTP reduces chronic pain.

Per the release, increased activity has been seen in the ACC in humans suffering from anxiety disorders and in animal models of anxiety. However, how LTP in the ACC differs in chronic pain, or why the two would interact to result in more pain in anxiety sufferers and more anxiety in pain sufferers, was not known.

The most common form of LTP, according to the release, is post-LTP. Another form of LTP is called pre-LTP, and it occurs before the synapse and involves the release of a larger amount of the signal from the neuron upstream, the release explains.

By using molecules that specifically block pre-LTP or post-LTP, Zhuo and his team suggest that they found a new form of pre-LTP that occurs in the ACC. Pre-LTP had previously only been seen in other brain regions.

They also suggest that pre-LTP and post-LTP were present in conditions of chronic pain, but that pre-LTP was only present when the pain became chronic, and not in cases of acute pain, according to the release.

Additionally, the researchers indicate that blocking pre-LTP reduced anxiety, and also that conditions that produced anxiety in animals (without pain) resulted in pre-LTP. Per the release, these findings led the researchers to the suggested conclusion that pre-LTP in neurons of the ACC mediates anxiety.

The release notes that Zhuo and his team also found a novel molecule, called NB001, which can specifically block neuronal pre-LTP and has powerful pain-reducing effects in animal models of chronic pain.

“As compared with post-LTP, pre-LTP employs a different set of molecules to induce and express the injury-related potentiation,” Zhuo says.

It also paves the way for new opportunities to discover treatments that may selectively control anxiety vests pain in the future, Zhu adds.

[Source: Canadian Association for Neuroscience]