About this Research Topic
This Research Topic is the second volume of the Research Topic "Molecular Mechanism of Neuroimmune Modulation and Synaptic Plasticity in Acute and Chronic Pain". Please see the first volume here.
Pain is a common, complex, and unpleasant sensation followed by nerve injury, tissue trauma, inflammatory diseases, infection, cancer, and drug exposure. Patients with pain often experience insomnia, depression, anxiety, and cognitive impairments, which are known to be associated with worsening pain and a serious threat to their quality of life. Pain is also often refractory to most current analgesics, thus emphasizing the requirement for improved therapeutic medications. It is of great importance to elucidate the specific molecular pathogenesis of acute and chronic pain with different etiologies. Also, it is of great interest to discuss the interaction between sleep disorders and pain states.
In the past decades, we have witnessed exciting discoveries that the interaction between neurons and glial cells (microglia and astrocyte) contributes to peripheral and central sensitization of nociceptive circuitry, which governs multiple pain perceptions and synaptic plasticity. Chemokine-induced neuroinflammation is identified to be a critical step for glial cells activation. The activation of excitatory glutaminergic receptors is a cardinal feature of nociceptive synaptic plasticity. Yet, the specific molecular and cellular mechanisms underlying neuroimmune regulation, synaptic plasticity, and pain development remain unclear and attract considerable attention.
This Research Topic is designated to collect Original Research, Review, and Perspective articles to further our understanding of novel pain-associated molecules and their signaling pathways, which can be used as therapeutic targets for pain treatment. The sub-themes of this Research Topic include but are not limited to:
• Novel molecules and their roles in neuroinflammation and pain processing;
• Studies on chemokines, inflammatory mediators, microglia-activating factors, postsynaptic proteins, and ion channels, which are implicated in pain sensitization;
• Identification of potential therapeutic targets and pathological mechanisms of pain with different etiologies;
• Recent insights into the pathophysiology of sex dimorphism in pain and neuroinflammation;
• Recent insights into the monitoring methods of nociception during surgery;
• Pain-related clinical research protocols and research papers;
• Mechanisms by which sleep deprivation exacerbates neuropathic pain.
Pain is a common, complex, and unpleasant sensation followed by nerve injury, tissue trauma, inflammatory diseases, infection, cancer, and drug exposure. Patients with pain often experience insomnia, depression, anxiety, and cognitive impairments, which are known to be associated with worsening pain and a serious threat to their quality of life. Pain is also often refractory to most current analgesics, thus emphasizing the requirement for improved therapeutic medications. It is of great importance to elucidate the specific molecular pathogenesis of acute and chronic pain with different etiologies. Also, it is of great interest to discuss the interaction between sleep disorders and pain states.
In the past decades, we have witnessed exciting discoveries that the interaction between neurons and glial cells (microglia and astrocyte) contributes to peripheral and central sensitization of nociceptive circuitry, which governs multiple pain perceptions and synaptic plasticity. Chemokine-induced neuroinflammation is identified to be a critical step for glial cells activation. The activation of excitatory glutaminergic receptors is a cardinal feature of nociceptive synaptic plasticity. Yet, the specific molecular and cellular mechanisms underlying neuroimmune regulation, synaptic plasticity, and pain development remain unclear and attract considerable attention.
This Research Topic is designated to collect Original Research, Review, and Perspective articles to further our understanding of novel pain-associated molecules and their signaling pathways, which can be used as therapeutic targets for pain treatment. The sub-themes of this Research Topic include but are not limited to:
• Novel molecules and their roles in neuroinflammation and pain processing;
• Studies on chemokines, inflammatory mediators, microglia-activating factors, postsynaptic proteins, and ion channels, which are implicated in pain sensitization;
• Identification of potential therapeutic targets and pathological mechanisms of pain with different etiologies;
• Recent insights into the pathophysiology of sex dimorphism in pain and neuroinflammation;
• Recent insights into the monitoring methods of nociception during surgery;
• Pain-related clinical research protocols and research papers;
• Mechanisms by which sleep deprivation exacerbates neuropathic pain.
Keywords: pain, neuroinflammation, glial activation, peripheral sensitization, central sensitization, synaptic plasticity, chemokine, opioid induced tolerance and hyperalgesia, pain monitoring methods, neuropathic pain, sleep deprivation, oxidative stress, sleep disorder
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