Summary: A new study reveals that neurons in the brain trunk respond very differently to acute pain versus chronic pain, which can explain why certain pain persists long after the lesion. In acute pain, neurons in the medullary dorsal horn reduce their activity through a natural “braking” system that involves potassium currents of type A, which helps limit pain signs.
But in chronic pain, this mechanism fails, and neurons become hyperactive, continuing sending pain messages. This discovery provides a clearer biological route on how pain becomes chronic and can guide future therapies aimed at restoring this internal regulation system.
Key facts:
Dysfunction of the brain trunk relay: in chronic pain, neurons in the medullary dorsal horn lose their ability to cushion pain signs.
Source: Hebrew University of Jerusalem
Why does a pain disappear while other types persist, becoming chronic suffering?
An innovative study of scientists from the Hebrew University of Jerusalem may have discovered part of the response, at the bottom of the brainstem.
In a study published this week in scientific advances, researchers led by the Title of Doctorate Ben Ben title under the guidance of Prof. Alexander M. Binshtok of the Hebrew School of Medicine of the University-HusiShNSH and the Center for Cerebro Sciences (ELSC), reveal that our bodies respond to the acute (short-term) and chronic level (long) (long) in a surprisingly different way at a cellular level.
Its discovery sheds new light on how pain becomes chronic and opens the door to better directed treatments.
The “pain relays” of the brain behave differently in acute pain against chronic pain
The team studied a small but crucial region in the brain trunk called a medullary horn, home of neurons that act as a relay station for pain signals. These projection neurons help send messages of body pain to the brain.
The scientists found that during acute inflammatory pain, these neurons actually charge their own activity. This “braking system” incorporated helps to limit the amount of pain related to the pain sent to the brain. Once inflammation and pain decrease, neurons return to their normal state.
However, in chronic pain, this braking system fails. Neurons do not reduce their activity; In fact, they become more excitable and shoot more signals, potentially contributing to the persistence of pain.
The key player: type A potassium
Using a combination of electrophysiology and computer modeling, the researchers identified a key mechanism: a specific potassium stream known as type A potassium current (AI). This current helps regulate the excitability of neurons.
In acute pain, it increases, acting as a natural sedative for pain paths. But in chronic pain, this current does not increase and neurons become hyperactive. The absence of this regulation can be one of the biological switches that converts temporary pain into a lasting condition.
Implications for chronic pain treatment
“This is the first time we see how the same neurons behave so differently in acute pain versus chronic,” said Professor Binshtok.
“The fact that this ‘soothing’ natural mechanism is missing in chronic pain suggests a new objective for therapy. If we can find a way to restore or imitate that braking system, we could prevent pain from being chronic.”
A step towards smarter pain therapies
Chronic pain affects more than 50 million people only in the US, often with few effective treatment options. This new study adds an important piece to the puzzle by showing how the pains of pain incorporated from the nervous system are interrupted in long -term pain conditions.
By understanding the brain’s own strategies to limit pain, and why sometimes they fail, scientists are now one step closer to develop more intelligent and precise therapies for those who suffer chronic pain.
On this pain and neuroscience research news
Author: Danae Marx
Source: Hebrew University of Jerusalem
Contact: Danae Marx – Hebrew University of Jerusalem
Image: The image is accredited to Neuroscience News
Original research: open access.
“Opposite regulation of the excitability of the medullary projection neuron related to pain in acute and chronic pain” by Alexander M. Binshtok et al. Scientific advances
Abstract
Opposite regulation of the excitability of medullary projection neurons related to pain in acute and chronic pain
Hypersensitivity to pain is associated with greater activity of peripheral and central neurons along pain neuroaxis.
We show that in the peak of acute inflammatory pain, the projection neurons of the superficial core dorsal horn (PNS) that transmit nociceptive information to the parabrachial nucleus reduce its intrinsic excitability and, consequently, the potential trigger for action.
When the pain is resolved, the excitability of these neurons returns to the baseline.
Using electrophysiological and computational approaches, we find that an increase in potassium current (AI) underlies the decrease in the excitability of medullary SNPs of the dorsal horn in acute pain conditions.
In chronic pain conditions, no changes to AI were observed, and the dorsal horns medullants exhibit greater intrinsic excitability and shot.
Our results reveal a differential modulation of the excitability of the projection neurons of the medullary dorsal horn in conditions of acute and chronic pain, which suggests a regulatory mechanism that, in acute pain conditions, tune in the production of the dorsal horn and, if it is not, could facilitate the chronification of pain.
