A new study reveals that when we experience short-term (acute) pain, the brain has a built‑in way to dial down pain signals—like pressing the brakes—to keep them from going into overdrive. But in long‑term (chronic) pain, this braking system fails, and the pain signals just keep firing. This discovery helps explain why some pain goes away while other pain lingers, and it opens the door to new treatments that could stop pain from becoming chronic in the first place.
In a study published in Science Advances, researchers—led by Doctoral student Ben Title under the guidance of Prof. Alexander M. Binshtok from The Hebrew University-Hadassah School of Medicine and the Center for Brain Sciences (ELSC) at The Hebrew University—reveal that our bodies respond to acute (short‑term) and chronic (long‑lasting) pain in surprisingly different ways at the cellular level. Their discovery sheds new light on how pain becomes chronic—and opens the door to better‑targeted treatments.
The brain’s pain relays behave differently in acute vs. chronic pain
The team studied a small but crucial region in the brainstem called the medullary dorsal horn, home to neurons that act as a relay station for pain signals. These projection neurons help send pain messages from the body to the brain.
The scientists found that during acute inflammatory pain, these neurons actually dial down their own activity. This built‑in “braking system” helps limit the amount of pain‑related signals sent to the brain. Once the inflammation and pain subside, the neurons return to their normal state.
However, in chronic pain, this braking system fails. The neurons don’t reduce their activity—in fact, they become more excitable and fire more signals, potentially contributing to the persistence of pain.
The key player: A‑type potassium current
Using a combination of electrophysiology and computer modeling, the researchers identified a key mechanism: a specific potassium current known as the A‑type potassium current (IA). This current helps regulate the excitability of neurons.
In acute pain, IA increases—acting like a natural sedative for the pain pathways. But in chronic pain, this current doesn’t ramp up, and the neurons become hyperactive. The absence of this regulation may be one of the biological switches that turns temporary pain into a long‑lasting condition.
“This is the first time we’ve seen how the same neurons behave so differently in acute versus chronic pain,” said Prof. Binshtok. “The fact that this natural ‘calming’ mechanism is missing in chronic pain suggests a new target for therapy. If we can find a way to restore or mimic that braking system, we might be able to prevent pain from becoming chronic.”
A step toward smarter pain therapies
Chronic pain affects over 50 million people in the U.S. alone, often with few effective treatment options. This new study adds an important piece to the puzzle by showing how the nervous system’s built‑in pain controls are disrupted in long‑term pain conditions.
By understanding the brain’s own strategies for limiting pain—and why they sometimes fail—scientists are now one step closer to developing smarter, more precise therapies for those who suffer from chronic pain.
More information:
Ben Title et al, Opposite regulation of medullary pain-related projection neuron excitability in acute and chronic pain, Science Advances (2025). DOI: 10.1126/sciadv.adr3467. www.science.org/doi/10.1126/sciadv.adr3467
Citation:
Why acute and chronic pain are so different—and what might make pain last (2025, June 20)
retrieved 20 June 2025
from https://medicalxpress.com/news/2025-06-acute-chronic-pain.html
This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no
part may be reproduced without the written permission. The content is provided for information purposes only.
A new study reveals that when we experience short-term (acute) pain, the brain has a built‑in way to dial down pain signals—like pressing the brakes—to keep them from going into overdrive. But in long‑term (chronic) pain, this braking system fails, and the pain signals just keep firing. This discovery helps explain why some pain goes away while other pain lingers, and it opens the door to new treatments that could stop pain from becoming chronic in the first place.
In a study published in Science Advances, researchers—led by Doctoral student Ben Title under the guidance of Prof. Alexander M. Binshtok from The Hebrew University-Hadassah School of Medicine and the Center for Brain Sciences (ELSC) at The Hebrew University—reveal that our bodies respond to acute (short‑term) and chronic (long‑lasting) pain in surprisingly different ways at the cellular level. Their discovery sheds new light on how pain becomes chronic—and opens the door to better‑targeted treatments.
The brain’s pain relays behave differently in acute vs. chronic pain
The team studied a small but crucial region in the brainstem called the medullary dorsal horn, home to neurons that act as a relay station for pain signals. These projection neurons help send pain messages from the body to the brain.
The scientists found that during acute inflammatory pain, these neurons actually dial down their own activity. This built‑in “braking system” helps limit the amount of pain‑related signals sent to the brain. Once the inflammation and pain subside, the neurons return to their normal state.
However, in chronic pain, this braking system fails. The neurons don’t reduce their activity—in fact, they become more excitable and fire more signals, potentially contributing to the persistence of pain.
The key player: A‑type potassium current
Using a combination of electrophysiology and computer modeling, the researchers identified a key mechanism: a specific potassium current known as the A‑type potassium current (IA). This current helps regulate the excitability of neurons.
In acute pain, IA increases—acting like a natural sedative for the pain pathways. But in chronic pain, this current doesn’t ramp up, and the neurons become hyperactive. The absence of this regulation may be one of the biological switches that turns temporary pain into a long‑lasting condition.
“This is the first time we’ve seen how the same neurons behave so differently in acute versus chronic pain,” said Prof. Binshtok. “The fact that this natural ‘calming’ mechanism is missing in chronic pain suggests a new target for therapy. If we can find a way to restore or mimic that braking system, we might be able to prevent pain from becoming chronic.”
A step toward smarter pain therapies
Chronic pain affects over 50 million people in the U.S. alone, often with few effective treatment options. This new study adds an important piece to the puzzle by showing how the nervous system’s built‑in pain controls are disrupted in long‑term pain conditions.
By understanding the brain’s own strategies for limiting pain—and why they sometimes fail—scientists are now one step closer to developing smarter, more precise therapies for those who suffer from chronic pain.
More information:
Ben Title et al, Opposite regulation of medullary pain-related projection neuron excitability in acute and chronic pain, Science Advances (2025). DOI: 10.1126/sciadv.adr3467. www.science.org/doi/10.1126/sciadv.adr3467
Citation:
Why acute and chronic pain are so different—and what might make pain last (2025, June 20)
retrieved 20 June 2025
from https://medicalxpress.com/news/2025-06-acute-chronic-pain.html
This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no
part may be reproduced without the written permission. The content is provided for information purposes only.
