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Epileptiform activity and behavioral arrests in mice overexpressing the calcium channel subunit α2δ-1

Neurobiology of disease, 2017-06, Vol.102, p.70-80

2017

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Calcium channel alpha-2-delta-1 protein upregulation in dorsal spinal cord mediates spinal cord injury-induced neuropathic pain states

Pain (Amsterdam), 2011-03, Vol.152 (3), p.649-655

2011

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Central Mechanisms Mediating Thrombospondin-4-induced Pain States

The Journal of biological chemistry, 2016-06, Vol.291 (25), p.13335-13348

2016

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Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acetic protein in maintenance of pain behaviors

Pain (Amsterdam), 2009-05, Vol.143 (1), p.114-122

2009

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The EGF-LIKE domain of thrombospondin-4 is a key determinant in the development of pain states due to increased excitatory synaptogenesis

The Journal of biological chemistry, 2018-10, Vol.293 (42), p.16453-16463

2018

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Calcium channel functions in pain processing

Channels (Austin, Tex.), 2010-11, Vol.4 (6), p.510-517

2010

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Pathophysiological roles of thrombospondin-4 in disease development

Seminars in cell & developmental biology, 2024-03, Vol.155 (Pt B), p.66-73

2024

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Persistent inflammation alters the density and distribution of voltage-activated calcium channels in subpopulations of rat cutaneous DRG neurons

Pain (Amsterdam), 2010-12, Vol.151 (3), p.633-643

2010

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Injury discharges regulate calcium channel alpha-2-delta-1 subunit upregulation in the dorsal horn that contributes to initiation of neuropathic pain

Pain (Amsterdam), 2008-10, Vol.139 (2), p.358-366

2008

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Gabapentin Receptor α2δ-1 Is a Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis

Cell, 2009-10, Vol.139 (2), p.380-392

2009

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Targeting Voltage-Gated Calcium Channels for Neuropathic Pain Management

Neurotherapeutics, 2009-10, Vol.6 (4), p.679-692

2009

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Thrombospondin-4 and excitatory synaptogenesis promote spinal sensitization after painful mechanical joint injury

Experimental neurology, 2015-02, Vol.264, p.111-120

2015

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Painful nerve injury upregulates thrombospondin-4 expression in dorsal root ganglia

Journal of neuroscience research, 2015-03, Vol.93 (3), p.443-453

2015

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Calcium Channel α2δ1 Proteins Mediate Trigeminal Neuropathic Pain States Associated with Aberrant Excitatory Synaptogenesis

The Journal of biological chemistry, 2014-03, Vol.289 (10), p.7025-7037

2014

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Increased thrombospondin-4 after nerve injury mediates disruption of intracellular calcium signaling in primary sensory neurons

Neuropharmacology, 2017-05, Vol.117, p.292-304

2017

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Spinal Dorsal Horn Calcium Channel α2δ-1 Subunit Upregulation Contributes to Peripheral Nerve Injury-Induced Tactile Allodynia

The Journal of neuroscience, 2004-09, Vol.24 (39), p.8494-8499

2004

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Synaptic ultrastructure changes in trigeminocervical complex posttrigeminal nerve injury

Journal of comparative neurology (1911), 2016-02, Vol.524 (2), p.309-322

2016

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Application of Pulsed Radiofrequency Currents to Rat Dorsal Root Ganglia Modulates Nerve Injury-Induced Tactile Allodynia

Anesthesia and analgesia, 2011-09, Vol.113 (3), p.610-616

2011

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Coupling gene chip analyses and rat genetic variances in identifying potential target genes that may contribute to neuropathic allodynia development

Journal of neurochemistry, 2003-11, Vol.87 (3), p.560-573

2003

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Calcium channel α2δ1 subunit mediates spinal hyperexcitability in pain modulation

Pain (Amsterdam), 2006-11, Vol.125 (1-2), p.20-34

2006

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The monosodium iodoacetate model of osteoarthritis pain in the rat

Methods in molecular biology (Clifton, N.J.), 2012-01, Vol.851, p.239

2012

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The role of nitric oxide in nociception

Current pain and headache reports, 2000, Vol.4 (6), p.459-466

2000

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Injury‐induced maladaptation and dysregulation of calcium channel α2δ subunit proteins and its contribution to neuropathic pain development

British journal of pharmacology, 2018-06, Vol.175 (12), p.2231-2243

2018

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Corrigendum to “Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acidic protein in maintenance of pain behaviors” [Pain 143 (2009) 114–122]

Pain (Amsterdam), 2009-08, Vol.144 (3), p.345-345

2009

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Advancements in pain research

Methods in molecular biology (Clifton, N.J.), 2012, Vol.851, p.1

Luo, Z David

2012

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Epileptiform activity and behavioral arrests in mice overexpressing the calcium channel subunit α2δ-1

Calcium channel alpha-2-delta-1 protein upregulation in dorsal spinal cord mediates spinal cord injury-induced neuropathic pain states

Central Mechanisms Mediating Thrombospondin-4-induced Pain States

Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acetic protein in maintenance of pain behaviors

The EGF-LIKE domain of thrombospondin-4 is a key determinant in the development of pain states due to increased excitatory synaptogenesis

Calcium channel functions in pain processing

Pathophysiological roles of thrombospondin-4 in disease development

Persistent inflammation alters the density and distribution of voltage-activated calcium channels in subpopulations of rat cutaneous DRG neurons

Injury discharges regulate calcium channel alpha-2-delta-1 subunit upregulation in the dorsal horn that contributes to initiation of neuropathic pain

Gabapentin Receptor α2δ-1 Is a Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis

Targeting Voltage-Gated Calcium Channels for Neuropathic Pain Management

Thrombospondin-4 and excitatory synaptogenesis promote spinal sensitization after painful mechanical joint injury

Painful nerve injury upregulates thrombospondin-4 expression in dorsal root ganglia

Calcium Channel α2δ1 Proteins Mediate Trigeminal Neuropathic Pain States Associated with Aberrant Excitatory Synaptogenesis

Increased thrombospondin-4 after nerve injury mediates disruption of intracellular calcium signaling in primary sensory neurons

Spinal Dorsal Horn Calcium Channel α2δ-1 Subunit Upregulation Contributes to Peripheral Nerve Injury-Induced Tactile Allodynia

Synaptic ultrastructure changes in trigeminocervical complex posttrigeminal nerve injury

Application of Pulsed Radiofrequency Currents to Rat Dorsal Root Ganglia Modulates Nerve Injury-Induced Tactile Allodynia

Coupling gene chip analyses and rat genetic variances in identifying potential target genes that may contribute to neuropathic allodynia development

Calcium channel α2δ1 subunit mediates spinal hyperexcitability in pain modulation

The monosodium iodoacetate model of osteoarthritis pain in the rat

The role of nitric oxide in nociception

Injury‐induced maladaptation and dysregulation of calcium channel α2δ subunit proteins and its contribution to neuropathic pain development

Corrigendum to “Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acidic protein in maintenance of pain behaviors” [Pain 143 (2009) 114–122]

Advancements in pain research

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