Scientists at the Hebrew University of Jerusalem have discovered why acute pain fades while chronic pain persists. Their study, published in Science Advances, reveals that neurons in the brainstem dial down activity during acute pain but become hyperactive in chronic pain due to a failed “braking system.” This breakthrough could lead to new treatments targeting the root cause of chronic pain.
The research team, led by doctoral student Ben Title and Prof. Alexander M. Binshtok, focused on the medullary dorsal horn, a brainstem region that relays pain signals to the brain. They found that during acute inflammatory pain, neurons in this region reduce their activity, acting like a natural brake. However, in chronic pain, this mechanism fails, and the neurons fire excessively.
A key player in this process is the A-type potassium current (IA), which regulates neuron excitability. In acute pain, IA increases, calming the neurons. But in chronic pain, IA does not ramp up, leaving neurons hyperactive. This discovery explains why some pain becomes long-lasting and highlights a potential target for future therapies.
“This is the first time we’ve seen how the same neurons behave so differently in acute versus chronic pain,” said Prof. Binshtok. “Restoring this ‘braking system’ could prevent pain from becoming chronic.”
Chronic pain affects over 50 million people in the U.S., often with limited treatment options. By uncovering the brain’s failed pain-control mechanism, this study paves the way for more effective therapies. Future research will explore how to restore or mimic the IA current to halt chronic pain at its source.
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