Scientists Identify Neurons Responsible For Sustained Pain and Resulting Pain-Coping Behaviors

  • A new study confirms the presence of two different types of responses to injury: withdrawal reflex and pain-coping response.
  • Each response is controlled by separate nerve-signaling pathways.

Animals exhibit two types of response to painful stimuli. The first one is reflexive defensive responses to prevent or reduce injury. The perfect example of such responses is the quick withdrawal of hand upon touching an extremely hot surface.

When this type of response fails to prevent harm, the coping response comes into action. For example, licking the burned skin or pressing a banged toe to sooth the damaged area. However, the underlying mechanism that drives these two different behaviors remains poorly understood.

Now, the researchers at Harvard Medical School have found a nerve-signaling pathway responsible for sustained pain (that immediately follows injury) and resulting pain-coping behaviors.

So far, we’ve only observed distinct brain regions to study reflexive responses and long-lasting pain caused by injuries. The new research, on the other hand, maps out how such responses appear outside the brain.

Experiments Performed On Mice

Researchers focused on a specific type of neurons known as Tac1 emerging from the dorsal horn, a group of nerves in the spinal cord’s lower end that receives various sensory information from the body and transfers it to the brain.

To understand how Tac1 neurons actually work (or whether they are responsible for the sensation of sustained pain), researchers conducted a series of experiments on two groups of mice. The first group had intact Tac1 while the second group had chemically deactivated Tac1 neurons.

Reference: Nature | doi:10.1038/s41586-018-0793-8 | Harvard Medical School 

The second group showed usual withdrawal reflexes when exposed to a noxious stimulus (hot or cool object). However, when they were injected with burn-inducing mustard oil, they showed no paw licking behavior that other animals usually do immediately following injury.

They didn’t even show any pain-coping responses when researchers pinched their hind paws. By contrast, the first group of mice engaged in prolonged, vigorous paw licking to soothe the pain.

The observations indicate that Tac1 neurons do not affect reflexive reactions to external threats, but they play a crucial role in pain-coping behaviors.

The team also investigated whether Tac1 neurons is linked with another type of neurons, named Trpv1, that are present throughout the body and provides a sensation of scalding heat and pain.

Mice with intact Tac1 but chemically inactivated Trpv1 neurons showed weak reactions to pinch-induced pain: they showed less paw licking than usual. The finding confirms that Tac1 and Trvp1 neurons are connected to each other in the lower end of the spinal cord. And the connection gets activated when these neurons transfer their signals.

According to the researchers, Tac1 neurons send pain signal from the tissue through Trpv1 nerves all the way to the brain.

How It’s Useful?

The study questions the validity of existing experimental techniques for assessing the efficiency of pain-relief doses. Most current techniques measure reflexive responses, instead of measuring the sustained pain that emerges from tissue damage.

The finding explains why some drug components were unsuccessful in soothing long-lasting pain. All these years, we might have been focusing on the wrong response.

Read: 15 Mind-boggling Facts About The Nervous System

The study could help scientists translate the current treatments from preclinical studies into efficacious pain therapies. The process can also be conserved across several species to increase survival.

Written by
Varun Kumar

Varun Kumar is an experienced science and technology journalist interested in machines, AI, and space exploration. He received a Master's degree in computer science from Indraprastha University. To find out what his latest project is, feel free to directly email him at [email protected] 

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