Representative Publications
Cellular and Molecular Mechanisms of Chronic Pain
- Zhang J, Chen SR, Zhou MH, Jin D, Chen H, Wang L, DePinho RA, Pan HL. HDAC2 in Primary Sensory Neurons Constitutively Restrains Chronic Pain by Repressing α2δ-1 Expression and Associated NMDA Receptor Activity. J Neurosci. 2022 Nov 30;42(48):8918-8935. doi: 10.1523/JNEUROSCI.0735-22.2022.
- Li L, Chen SR, Zhou MH, Wang L, Li DP, Chen H, Lee G, Jayaraman V, Pan HL.
α2δ-1 switches the phenotype of synaptic AMPA receptors by physically disrupting heteromeric subunit assembly. Cell Rep. 2021 Jul 20;36(3):109396. doi: 10.1016/j.celrep.2021.109396. - Huang Y, Chen SR, Chen H, Luo Y, Pan HL. Calcineurin Inhibition Causes α2δ-1-Mediated Tonic Activation of Synaptic NMDA Receptors and Pain Hypersensitivity. J Neurosci. 2020 May 6;40(19):3707-3719. doi: 10.1523/JNEUROSCI.0282-20.2020.
- Chen J, Li L, Chen SR, Chen H, Xie JD, Sirrieh RE, MacLean DM, Zhang Y, Zhou MH, Jayaraman V, Pan HL. The α2δ-1-NMDA Receptor Complex Is Critically Involved in Neuropathic Pain Development and Gabapentin Therapeutic Actions. Cell Rep. 2018 Feb 27;22(9):2307-2321. doi: 10.1016/j.celrep.2018.02.021.
- Laumet G, Garriga J, Chen SR, Zhang Y, Li DP, Smith TM, Dong Y, Jelinek J, Cesaroni M, Issa JP, Pan HL. G9a is essential for epigenetic silencing of K(+) channel genes in acute-to-chronic pain transition. Nat Neurosci. 2015 Dec;18(12):1746-55. doi: 10.1038/nn.4165.
Mechanisms of Opioid-induced Analgesia and Adverse Effects
Journal of Biological Chemistry cover image, used under CC-BY license
- Chen SR, Chen H, Jin D, Pan HL. Brief Opioid Exposure Paradoxically Augments Primary Afferent Input to Spinal Excitatory Neurons via α2δ-1-Dependent Presynaptic NMDA Receptors. J Neurosci. 2022 Dec 14;42(50):9315-9329. doi: 10.1523/JNEUROSCI.1704-22.2022.
- Deng M, Chen SR, Chen H, Pan HL. α2δ-1-Bound N-Methyl-D-aspartate Receptors Mediate Morphine-induced Hyperalgesia and Analgesic Tolerance by Potentiating Glutamatergic Input in Rodents.
Anesthesiology. 2019 May;130(5):804-819. doi: 10.1097/ALN.0000000000002648. - Sun J, Chen SR, Chen H, Pan HL. μ-Opioid receptors in primary sensory neurons are essential for opioid analgesic effect on acute and inflammatory pain and opioid-induced hyperalgesia.
J Physiol. 2019 Mar;597(6):1661-1675. doi: 10.1113/JP277428. - Zhao YL, Chen SR, Chen H, Pan HL. Chronic opioid potentiates presynaptic but impairs postsynaptic N-methyl-D-aspartic acid receptor activity in spinal cords: implications for opioid hyperalgesia and tolerance. J Biol Chem. 2012 Jul 20;287(30):25073-85. doi: 10.1074/jbc.M112.378737.
- Zhou HY, Chen SR, Chen H, Pan HL. Opioid-induced long-term potentiation in the spinal cord is a presynaptic event. J Neurosci. 2010 Mar 24;30(12):4460-6. doi: 10.1523/JNEUROSCI.5857-09.2010.
Mechanisms of Neurogenic Hypertension
- Zhou JJ, Shao JY, Chen SR, Pan HL. Calcineurin Controls Hypothalamic NMDA Receptor Activity and Sympathetic Outflow. Circ Res. 2022 Aug 5;131(4):345-360. doi: 10.1161/CIRCRESAHA.122.320976.
- Zhou JJ, Shao JY, Chen SR, Li DP, Pan HL. α2δ-1-Dependent NMDA Receptor Activity in the Hypothalamus Is an Effector of Genetic-Environment Interactions That Drive Persistent Hypertension.
J Neurosci. 2021 Jul 28;41(30):6551-6563. doi: 10.1523/JNEUROSCI.0346-21.2021. - Ma H, Chen SR, Chen H, Pan HL. Endogenous AT1 receptor-protein kinase C activity in the hypothalamus augments glutamatergic input and sympathetic outflow in hypertension. J Physiol. 2019 Aug;597(16):4325-4340. doi: 10.1113/JP278427.
- Ma H, Chen SR, Chen H, Zhou JJ, Li DP, Pan HL.α2δ-1 couples to NMDA receptors in the hypothalamus to sustain sympathetic vasomotor activity in hypertension. J Physiol. 2018 Sep;596(17):4269-4283. doi: 10.1113/JP276394.
- Li DP, Zhou JJ, Zhang J, Pan HL. CaMKII Regulates Synaptic NMDA Receptor Activity of Hypothalamic Presympathetic Neurons and Sympathetic Outflow in Hypertension. J Neurosci. 2017 Nov 1;37(44):10690-10699. doi: 10.1523/JNEUROSCI.2141-17.2017.