About this Research Topic
Pain is the most common reason for seeking medical care. Chronic pain can result from multiple pathologies including trauma, metabolic alterations, or the adverse side effects of chemotherapy. Chronic itch is also prevalent and can be triggered by different skin and systemic disorders, neuropathies, and the intake of different drugs. The medical and socioeconomic costs attached to their treatment are huge. Altered perception of normally innocuous stimuli as painful or the onset of spontaneous pain are also prominent features of chronic pain states. In many instances, excessive nociceptive input is an essential component of chronic pain development. In other cases, alteration in the processing of these inputs at the central level seems to be at the core of pain chronification. Abnormal sensory input and altered spinal networks are also thought to play critical roles in chronic itch development. However, the nature of supraspinal modulatory systems for pain and itch and their level of convergence is still poorly resolved. It has also become well established that reciprocal communication between neurons and non-neuronal cells, in particular glial and immune cells, also plays a critical role in the development and persistence of aberrant noxious and pruritic signals. A deeper knowledge of the structural and functional changes taking place in neuronal circuits involved in the processing of pain and itch signals is essential for deciphering their mechanisms.
Chronic pain and chronic itch present a major unmet clinical problem. One of the most significant barriers to developing more effective treatments is our limited understanding of the central circuits that play critically important roles in the modulation and relay of sensory information. Recent advances in this field include the characterization of molecularly defined populations of sensory neurons, interneurons, and projection neurons, the dissection of spinal cord circuits involved in different forms of pain and itch, and the role of non-neuronal cells such as glia and immune cells in mechanisms of pain sensitization. The aim of this Research Topic is to provide insight into our current understanding of neural circuits involved in pain and itch processing. This is achieved through a combination of focused reviews and original research articles that add to these rapidly evolving fields.
In this Research Topic, we welcome submissions of either original research or focused reviews on structural and functional changes in the peripheral and central nervous system that could help us understand the development of chronic pain and itch, highlighting their potential translation into novel therapeutic strategies. We particularly welcome contributions that include, but are not limited to, the following themes:
• Transduction molecules for touch, pain, and itch, and their plasticity following injury and aging
• The molecular profiling of neurons in pain circuits and the logic of their cellular architecture
• Pain pharmacology
• Chemotherapy-induced neuropathy and other peripheral neuropathies
• The development and application of novel technologies to interrogate pain circuits
• The use of IPSCs and organoids for disease modeling of pain
• The interaction between glial cells, immune cells, and sensory nerve endings and how this communication leads to nociceptive signal modulation.
Keywords: Ion channels, nociception, spinal cord dorsal horn, inflammatory pain, neuropathic pain, migraine, neuroimmune interactions, optopharmacology, disinhibition, central sensitization, AAVs, itch, sensory afferents
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.