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Scientists Recreate Human Pain Pathway in a Lab

In a groundbreaking study conducted by Stanford Medicine, researchers have successfully recreated a crucial Human Nerve sensory pathway in a laboratory dish. This artificial nerve circuit, called an “assembloid,” replicates the transmission of pain signals from the skin through the spinal cord to the brain. For the first time, scientists have been able to non-invasively observe the complete human ascending sensory pathway, which is responsible for carrying pain sensations.

The model is composed of four interconnected organoids, each representing a vital part of the nervous system: the dorsal root ganglion, dorsal spinal cord, thalamus, and somatosensory cortex. Senior researcher Dr. Sergiu Pasca, who has pioneered the use of brain organoids, said this new approach could open the door to more accurate pain research and better treatments. “We can now model this pathway non-invasively,” Pasca noted. “That will, we hope, help us learn how to better treat pain disorders.”

Unlike previous studies using animals, which often have pain mechanisms that differ from humans, this assembloid gives scientists a more reliable platform for studying human-specific neurological responses.

Testing Pain Signals and Genetic Mutations

To evaluate the functionality of the assembloid, researchers introduced pain-inducing substances like capsaicin—the active compound found in chili peppers—into the sensory region. This triggered spontaneous waves of neural activity that traveled through the spinal, thalamic, and cortical sections, effectively simulating real Human Nerve pain transmission.

The study also demonstrated how genetic mutations affect pain perception. Researchers introduced variations in the Nav1.7 sodium channel, a protein found mainly in peripheral sensory neurons. Mutations in this channel are known to either heighten pain sensitivity or eliminate pain perception altogether. When the mutant, pain-hypersensitive version of Nav1.7 was introduced, the assembloid showed intensified, synchronized neural activity. In contrast, disabling Nav1.7 disrupted this coordination—though neurons still fired, the overall signal failed to pass smoothly through the system.

These findings underscore the critical role of specific genes in pain disorders and demonstrate the assembloid’s potential for studying both inherited conditions and drug responses.

Future Potential in Chronic Pain and Drug Development

Pain remains one of the most widespread and challenging health issues globally. In the U.S. alone, over 116 million people suffer from chronic pain. Yet current treatments are limited, often relying on repurposed drugs or opioids, which carry a high risk of addiction.

Stanford’s new assembloid model offers a promising platform for identifying safer, more effective pain therapies. By targeting the sensory neurons involved in initiating pain signals—rather than the brain’s reward centers, which opioids affect—researchers aim to develop drugs that block pain without addictive side effects.

While the assembloid doesn’t “feel” pain itself, it accurately transmits sensory signals that mirror human physiological responses. As the model matures, scientists plan to use it to study pain-related neurodevelopmental disorders such as autism, which is often associated with sensory hypersensitivity.