Research may lead to new therapeutic strategies for treating allodynia.
Allodynia, pain experienced from slight sensations, currently has very limited treatments.
Researchers recently discovered a sequence of events in the S1 cortex may contribute to this chronic pain, according to a study published in The Journal of Clinical Investigation.
"Direct manipulation of the S1 cortex has been shown to relieve neuropathic pain in humans and animals. This suggests the S1 cortex might act as a sort of central processing unit within the brain networks that mediate and/or sustain chronic neuropathic pain," study author Sun Kwang Kim stated in a press release. "We hypothesized that S1 astrocytes, a type of glial cell, may show functional changes following peripheral nerve injury, resulting in mechanical allodynia."
Researchers conducted the study using mice with a nerve injury in their leg.
Thin filaments were applied to the bottom of the paw and each response was measured.
During this analysis, researchers used live calcium ion imaging to track the activities of astrocytes in the S1 cortex.
It was found that the signaling pathways were only activated for 1 week after the injury and associated spine turnover. In addition, blocking the pathways suppressed mechanical allodynia.
Researchers found that activating the pathways resulted in allodynia, even when an injury was absent.
The results suggest that when S1 astrocytes are reawakened, it triggers the S1 circuit to rewire, which explains neuropathic mechanical allodynia.
"By revealing some of the underlying mechanisms, our study suggests that cortical changes may move beyond their utility as just diagnostic tools and serve as potential targets for therapeutics," study author Junichi Nabekura stated. "Appreciation of these astrocyte-mediated changes in cortical synaptic connections requires a paradigm shift in our understanding of neuropathic pain pathophysiology; one that may result in novel therapeutic strategies for treating the debilitating effects of allodynia."