Publications

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Fig 1B Brandner et al 2022 J Pain

Mechanical and Heat Hyperalgesia upon Withdrawal From Chronic Intermittent Ethanol Vapor Depends on Sex, Exposure Duration, and Blood Alcohol Concentration in Mice.

Brandner et al., J Pain (2023)

Fig 3B Nelson et al 2022 PNAC

Targeting Spinal neuropeptide Y Y1 receptor-expressing neurons are a pharmacotherapeutic target for the alleviation of neuropathic pain.

Nelson et al., PNAS (2022)

Fig 3E Cooper er al 2022

Postsurgical Latent Pain Sensitization Is Driven by Descending Serotonergic Facilitation and Masked by µ-Opioid Receptor Constitutive Activity in the Rostral Ventromedial Medulla.

Cooper et al., JNeurosci (2022)

Fig 2A Cooper et al 2022 JNResearch

Endogenous µ-opioid receptor activity in the lateral and capsular subdivisions of the right central nucleus of the amygdala prevents chronic postoperative pain.

Cooper et al., JNResearch (2022)

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Facilitation of Neuropathic Pain by the NPY Y1 Receptor-Expressing Subpopulation of Excitatory Interneurons in the Dorsal Horn

Nelson et al., Science Reports (2019)

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Methylglyoxal and a Spinal TRPA1 AC1-Epac Cascade Facilitate Pain in the Db/Db Mouse Model of Type 2 Diabetes

Griggs et al., Neurobiology of Disease (2019)

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Fingolimod reduces neuropathic pain behaviors in a mouse model of multiple sclerosis by a sphingosine-1 phosphate receptor 1-dependent inhibition of central sensitization in the dorsal horn

Doolen et al., Pain (2018)

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Complement 3a receptor in dorsal horn microglia mediates pronociceptive neuropeptide signaling

Doolen et al., Glia (2017)

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Pioglitazone Inhibits the Development of Hyperalgesia and Sensitization of Spinal Nociresponsive Neurons in Type 2 Diabetes

Griggs et al., Journal of Pain (2016)

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Endogenous analgesia, dependence, and latent pain sensitization

Taylor BK and Corder G, Current Topics in Behavioral Neurosciences (2014)

Immunostained fluorescence microscopy image of a neuronal activation biomarker (phosphorylated extracellular regulated kinase, red) that increases in mouse spinal cord neurons (green) during opioid receptor inverse agonism. Inflammation or injury to the skin causes μ-opioid receptors to become constitutively active, which leads to long-term relief from chronic pain, but at the expense of endogenous opioid dependence.

Constitutive μ-opioid receptor activity leads to long-term endogenous analgesia and dependence

Corder et al.,  Science (2013)

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Tonic inhibition of chronic pain by neuropeptide Y

Solway et al., PNAS (2011)

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A novel method to quantify histochemical changes throughout the mediolateral axis of the substantia gelatinosa after spared nerve injury: characterization with TRPV1 and substance P

Corder et al., Journal of Pain (2010)

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