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Articles by Chen SR
Presynaptic Enhancement of Transmission from Nociceptors Expressing Nav1.8 onto Lamina-I Spinothalamic Tract Neurons by Spared Nerve Injury in Mice
brain slices chronic pain optogenetics spinal cord synaptic plasticity Significance Statement Altered synaptic function in the dorsal horn (DH) has been suggested as a possible cellular substrate for neuropathic pain. However, the type of synapse involved remains unclear. This study uses optogenetics to activate Nav1.8-expressing nociceptors and retrograde fluorescence tracing for whole-cell recordings from spinothalamic tract neurons (STTNs).
Etiology and Pharmacology of Neuropathic Pain
I. Introduction Pain is the most common reason for people to seek medical attention (Salter, 2014). Despite this, nociceptive pain is a vital physiologic process that signals actual or potential tissue damage (Iadarola and Caudle, 1997). By so doing, it protects the individual from injury and secures the survival of the species.
Imaging in Interventional Radiology: 2043 and Beyond
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Surface Inactivation of Highly Mutated SARS-CoV-2 Variants of Concern: Alpha, Delta, and Omicron
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NMDA Receptors at Primary Afferent-Excitatory Neuron Synapses Differentially Sustain Chemotherapy- and Nerve Trauma-Induced Chronic Pain
α2δ-1 dorsal root ganglion spinal cord K-Cl cotransporter-2 (KCC2) synaptic plasticity synaptic transmission Introduction Chronic neuropathic pain is often caused by peripheral nerve injury and certain cancer therapeutics. Both traumatic nerve injury and chemotherapy-induced neuropathy augment glutamate NMDAR activity in the spinal cord dorsal horn, which serves to amplify nociceptive input from primary sensory neurons (Woolf and Salter, 2000; H. Y. Zhou et al., 2011; Deng et al., 2019a).
The α2δ-1-NMDA receptor complex and its potential as a therapeutic target for ischemic stroke
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[Causal links between long-term exposure to NO2 and the risk of cardiovascular hospitalization]
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