F A C U L T Y   P R O F I L E 


Assistant Professor of Anesthesiology and Pharmacology

Cellular and molecular mechanisms of chronic pain.

Office: Black Building | Room 1111
Telephone: 212.305.1274
Fax: 212.304.6539

Current Research

Acute pain serves an important protective function: it is a physiological response to harmful environmental or internal stimuli that signals imminent tissue damage. In contrast, persistent pain caused by inflammation or injury to the nervous system is a debilitating disorder in urgent need of improved treatment.

My laboratory studies the pathophysiology of peripheral neuropathies associated with chronic pain. One of our main interests is the inflammatory response to peripheral nerve injury. We examine molecular messages that neurons, immune cells and glia exchange with each other. The goal is to determine the signals that trigger recruitment and activation of immune and glial cells, and examine how signals released from immune or glial cells modulate neuronal activity and contribute to the development of neuropathic pain. We further investigate how nerve injury disrupts the balance of excitation and inhibition in the dorsal horn of the spinal cord, which is a critical relay station for somatosensory information including pain. Normally, the processing of nociceptive input is tightly regulated. Peripheral nerve lesions lead to a loss of spinal inhibition through both dynamic and irreversible changes in the circuitry of local interneurons. This decrease in inhibition impairs the precise transmission of the location, intensity and duration of painful stimulation.

More recently, we have begun to study the mechanisms responsible for nerve damage in chemotherapy-induced or diabetic peripheral neuropathy. We utilize both in vitro and in vivo models of these diseases to evaluate innovative strategies for neuroprotection and pain treatment.

Selected Publications

1. Scholz J, Rathmell JP, David WS, Chad DA, Broderick AC, Perros SG, Shin NS, Wells JL, Davis JB, DiMaggio CJ, Wang S, Tate SN. A standardized clinical evaluation of phenotypic diversity in diabetic polyneuropathy. Pain 2016; 157(10):2297–308.

2. Yang F, Whang J, Derry WT, Vardeh D, Scholz J, Analgesic treatment with pregabalin does not prevent persistent pain after peripheral nerve injury in the rat. Pain 2014; 155(2):356–66

3. Inquimbert P, Bartels K, Babaniyi OB, Barrett LB, Tegeder I, Scholz J. Peripheral nerve injury produces a sustained shift in the balance between glutamate release and uptake in the dorsal horn of the spinal cord. Pain 2012; 153(12):2422–31 (PMC3540793)

4. Scholz J, Yaksh TL. Preclinical research on persistent postsurgical pain: what we don’t know, but should start studying. Anesthesiology 2010; 112:511–3 (PMC2828501)

5. Scholz J, Mannion RJ, Hord ED, Griffin RS, Rawal B, Zheng H, Scoffings D, Phillips A, Guo J, Laing RJC, Abdi S, Decosterd I, Woolf CJ. A Novel tool for the assessment of pain: validation in low back pain. PLoS Med 2009; 6(4):e1000047 (PMC2661253)

6. Scholz J, Woolf CJ. The neuropathic pain triad: neurons, immune cells, and glia. Nat Neurosci 2007; 10(11):1361–8

7. Scholz J, Broom DC, Youn DH, Mills CD, Kohno T, Suter MR, Moore KA, Decosterd I, Coggeshall RE, Woolf CJ. Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury. J Neurosci 2005; 25(32):7317–23

8. Tegeder I, Costigan M, Griffin RS, Abele A, Belfer I, Schmidt H, Ehnert C, Nejim J, Marian C, Scholz J, Wu T, Allchorne A, Diatchenko L, Binshtok A, Goldman D, Adolph J, Sama S, Atlas SJ, Carlezon WA, Parsegian A, Lötsch J, Fillingim RB, Maixner W, Geisslinger G, Max MB, Woolf CJ. GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistence. Nat Med 2006; 12(11):1269–77.

9. Scholz J, Woolf CJ. Can we conquer pain? Nat Neurosci 2002; 5 (Suppl):1062–7