Chronic Pain: New Signaling Discovery & Treatments
- Proteins known as calcium channels play a key role in transmitting pain signals through the nervous system.
- The nervous system primarily uses electrical signals to relay pain and other details.
- The Linköping University study centered on the CaV2.2 calcium channel, wich is involved in transmitting pain signals and becomes more active during chronic pain.
Linköping University scientists have made a breakthrough in understanding how calcium channels transmit chronic pain signals. Their discovery pinpoints the exact location within the CaV2.2 channel that modulates pain intensity. This research delves deep into the molecular mechanisms, offering hope for more targeted and effective chronic pain treatments. Currently, many drugs offer limited relief or come with harsh side effects. This study suggests a new approach: fine-tuning calcium channel activity rather than complete blockage like current methods. This could lead to innovative solutions for people suffering from debilitating conditions. News Directory 3 is following this story closely. Discover what’s next in the quest for pain relief with more tailored drugs.
New Insights into calcium Channels for Chronic Pain Relief
Updated June 22, 2025
Proteins known as calcium channels play a key role in transmitting pain signals through the nervous system. Now, researchers at Linköping University in Sweden have located the precise spot on a specific calcium channel that fine-tunes the intensity of these signals. This finding could pave the way for developing more effective chronic pain drugs with fewer side effects.
The nervous system primarily uses electrical signals to relay pain and other details. Though, at crucial points, these signals convert to biochemical forms using specific molecules. Understanding the molecular-level details of this conversion is essential for creating future pain medications. Voltage-sensitive calcium channels are of particular interest in this process. These channels act like molecular machines, detecting electrical signals and opening to allow calcium ions into nerve cells.
The Linköping University study centered on the CaV2.2 calcium channel, wich is involved in transmitting pain signals and becomes more active during chronic pain. These channels are located at the ends of sensory nerve cells. Current drugs that block CaV2.2 completely have severe side effects, requiring direct administration into the spinal fluid. Other drugs, like gabapentin, are not effective enough in reducing chronic pain. Opioids,such as morphine and heroin,exploit a natural mechanism to decrease CaV2.2’s response to pain signaling, but they are highly addictive.
“Calcium channels are very attractive drugs targets for pain treatment, but today’s solutions are inadequate,” said antonios Pantazis, associate professor at the Department of Biomedical and Clinical Sciences at linköping University, who led the study published in Science Advances.
The research team investigated how opioids reduce CaV2.2 activity. opioids release G proteins, which bind directly to calcium channels, making them less likely to open. The researchers discovered that G-proteins affect specific voltage sensors within the calcium channel, making them less responsive to electrical signals.
“It is as if G-protein signalling causes the channel to need more ‘persuasion’ — in terms of stronger electrical signals — to open. In our study, we describe at the molecular level how this is done,” Pantazis said.
The researchers used light-emitting molecules to track the movement of voltage sensors in response to electrical signals. They found that G-proteins impact the function of specific voltage sensors,but not others,making them more “reluctant” to sense electrical signals.
“Our finding points to a very specific part of the large calcium channel that next-generation drugs can target to provide pain relief in a similar way to opioids,” Pantazis said. “Instead of blocking the calcium channel completely, which is a less refined method, future drugs can be designed to fine-tune calcium channel activity in pain signalling.”
What’s next
The researchers hope that future drugs targeting the CaV2.2 calcium channel will provide better pain relief with fewer side effects. The study was funded by the Knut and Alice Wallenberg Foundation, the Swedish Brain Foundation, the Swedish Research Council, the National Institute of General Medical Sciences, and Lions Forskningsfond.