The sensation of pain is of enormous value to an organism; it allows a timely response to a potential damaging stimulus as well as the capability of learning new environmental dangers. On the other hand, pain persisting beyond the healing period of the initial damage, has no biological function and is maladaptive.
The dorsal horn of the spinal cord is the first processing location for pain signals before they are transmitted to the brain by ascending pathways. Along with the local circuitry, nociceptive information transfer in the spinal cord is also modulated by descending pathways. These may facilitate or attenuate pain and thus are thought to be involved in the establishment of persistent pain.
Multiple regions are involved in the processing of these signals at the brain level. The somatosensory cortex for example, plays a role in the sensory-discriminative aspects of pain, while affective-motivational aspects of pain are processed in limbic regions, such as in the amygdala. Although a specific and unique pain center area has not been identified yet, general consensus acknowledges that final pain perception is shaped by processing in multiple brain sites.
Neural plasticity, circuitry rewiring, and neuronal cell properties alterations, involved in both spinal and supraspinal processing of pain, are believed to lead to altered sensation and pain chronification during disease.
For instance, experimental evidence supports that alterations in chloride homeostasis in dorsal horn neurons in neuropathic pain, lead to an increase in excitatory activity, resulting in an enhanced pain sensitivity.
On the other hand, recent data in mouse models of neuropathic pain show attenuation of mPFC excitability in chronic pain, which is associated with a decrease in inhibitory descending activity contributing to pain hypersensitivity.
This Research Topic aims to broaden our understanding of neural circuits’ function and involvement in acute pain sensation or chronic pain conditions.
We welcome original research articles and review articles enriching our current knowledge on the cellular, synaptic and circuit mechanisms of acute and chronic pain.
We welcome articles addressing the following:
· Experimental evidence from in vivo and in vitro studies focusing on local pain circuits in different animal models
· Cell types and respective synaptic properties involved in acute or chronic pain
· Evidence of synaptic connectivity between CNS areas involved in pain states and pain perception
· Functional and structural synaptic plasticity in the context of pain: pre- and post- synaptic involvement and impact on pain circuitry modulation
