186 results on '"Chen, Shao-Rui"'
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2. Brain α2δ-1–Bound NMDA Receptors Drive Calcineurin Inhibitor–Induced Hypertension
3. mGluR5 from Primary Sensory Neurons Promotes Opioid-Induced Hyperalgesia and Tolerance by Interacting with and Potentiating Synaptic NMDA Receptors
4. Gene therapy approaches to restore chloride homeostasis for treating neuropathic pain
5. Contributors
6. The α2δ-1-NMDA receptor complex and its potential as a therapeutic target for ischemic stroke
7. Duloxetine and Amitriptyline Reduce Neuropathic Pain by Inhibiting Primary Sensory Input to Spinal Dorsal Horn Neurons via α1- and α2-Adrenergic Receptors
8. Brief Opioid Exposure Paradoxically Augments Primary Afferent Input to Spinal Excitatory Neurons via α2δ-1–Dependent Presynaptic NMDA Receptors
9. α2δ‐1 protein drives opioid‐induced conditioned reward and synaptic NMDA receptor hyperactivity in the nucleus accumbens
10. HDAC2 in Primary Sensory Neurons Constitutively Restrains Chronic Pain by Repressing α2δ-1 Expression and Associated NMDA Receptor Activity
11. δ-Opioid receptors in primary sensory neurons tonically restrain nociceptive input in chronic pain but do not enhance morphine analgesic tolerance
12. Calcineurin Controls Hypothalamic NMDA Receptor Activity and Sympathetic Outflow
13. NMDA Receptors and Signaling in Chronic Neuropathic Pain
14. Cannabinoid CB2 receptors are upregulated via bivalent histone modifications and control primary afferent input to the spinal cord in neuropathic pain
15. Calcineurin inhibition causes persistent hypertension through hypothalamic NMDA receptor‐dependent sympathetic outflow
16. Corrigendum to “LRRC8A-dependent volume-regulated anion channels contribute to ischemia-induced brain injury and glutamatergic input to hippocampal neurons” [Experimental Neurology, 332(2020)113391]
17. α2δ‐1 protein promotes synaptic expression of Ca 2+ permeable– AMPA receptors by inhibiting GluA1 / GluA2 heteromeric assembly in the hypothalamus in hypertension
18. The α2δ-1-NMDA Receptor Complex Is Critically Involved in Neuropathic Pain Development and Gabapentin Therapeutic Actions
19. Theta-Burst Stimulation of Primary Afferents Drives Long-Term Potentiation in the Spinal Cord and Persistent Pain via α2δ-1-Bound NMDA Receptors
20. Calcineurin Regulates Synaptic Plasticity and Nociceptive Transmission at the Spinal Cord Level
21. Regulation of Nociceptive Transduction and Transmission by Nitric Oxide
22. α2δ-1–Dependent NMDA Receptor Activity in the Hypothalamus Is an Effector of Genetic-Environment Interactions That Drive Persistent Hypertension
23. Protein Kinase C-Mediated Phosphorylation and α2δ-1 Interdependently Regulate NMDA Receptor Trafficking and Activity
24. LRRC8A-dependent volume-regulated anion channels contribute to ischemia-induced brain injury and glutamatergic input to hippocampal neurons
25. Group III metabotropic glutamate receptors regulate hypothalamic presympathetic neurons through opposing presynaptic and postsynaptic actions in hypertension
26. Calcineurin Inhibition Causes α2δ-1–Mediated Tonic Activation of Synaptic NMDA Receptors and Pain Hypersensitivity
27. Chronic Stress Induces Persistent Hypertension and Increases NMDA Receptor Activity in the Paraventricular Nucleus in Borderline Hypertensive Rats
28. Histone methyltransferase G9a diminishes expression of cannabinoid CB1 receptors in primary sensory neurons in neuropathic pain
29. μ-Opioid receptors in primary sensory neurons are involved in supraspinal opioid analgesia
30. Streptozotocin-Induced Diabetic Neuropathic Pain Is Associated with Potentiated Calcium-Permeable AMPA Receptor Activity in the Spinal Cord
31. Endogenous AT1 receptor–protein kinase C activity in the hypothalamus augments glutamatergic input and sympathetic outflow in hypertension
32. α2δ-1–BoundN-Methyl-d-aspartate Receptors Mediate Morphine-induced Hyperalgesia and Analgesic Tolerance by Potentiating Glutamatergic Input in Rodents
33. The &[Alpha]2δ‐1–NMDA Receptor Coupling is Essential for Corticostriatal Long‐Term Potentiation and is Involved in Learning and Memory
34. Endogenous transient receptor potential ankyrin 1 and vanilloid 1 activity potentiates glutamatergic input to spinal lamina I neurons in inflammatory pain
35. Synthesis and antiproliferative activity of novel 4-azasteroidal-17-hydrazone derivatives
36. Presynaptic NMDA receptors control nociceptive transmission at the spinal cord level in neuropathic pain
37. μ‐Opioid receptors in primary sensory neurons are essential for opioid analgesic effect on acute and inflammatory pain and opioid‐induced hyperalgesia
38. Increased α2δ‐1–NMDA receptor coupling potentiates glutamatergic input to spinal dorsal horn neurons in chemotherapy‐induced neuropathic pain
39. Mitogen‐activated protein kinase signaling mediates opioid‐induced presynaptic NMDA receptor activation and analgesic tolerance
40. RE1-silencing transcription factor controls the acute-to-chronic neuropathic pain transition and Chrm2 receptor gene expression in primary sensory neurons
41. The α2δ-1–NMDA receptor coupling is essential for corticostriatal long-term potentiation and is involved in learning and memory
42. Regulating nociceptive transmission by VGluT2-expressing spinal dorsal horn neurons
43. Focal Cerebral Ischemia and Reperfusion Induce Brain Injury Through α2δ-1–Bound NMDA Receptors
44. Reply to Meriney and Lacomis: Comment on direct aminopyridine effects on voltage-gated Ca2+ channels
45. α2δ-1 couples to NMDA receptors in the hypothalamus to sustain sympathetic vasomotor activity in hypertension
46. Synthesis of novel zinc porphyrins and their photocatalytic activity
47. α2δ-1 Is Essential for Sympathetic Output and NMDA Receptor Activity Potentiated by Angiotensin II in the Hypothalamus
48. Nerve Injury-Induced Chronic Pain Is Associated with Persistent DNA Methylation Reprogramming in Dorsal Root Ganglion
49. α2δ‐1 Is Essential for Angiotensin II‐Induced Sympathoexcitation and NMDA Receptor Hyperactivity in the Hypothalamus
50. The α2δ-1-NMDA Receptor Complex Is Critically Involved in Neuropathic Pain Development and Gabapentin Therapeutic Actions
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