It is the long-term objective of this laboratory to improve functional outcome after spinal cord injury (SCI). One important issue is the chronic pain sensations that the majority of patients with SCI experience. This project focuses on the development of a mammalian model of chronic central pain that is reproducible and has both spontaneous and evoked pain components, an important contribution which will allow an investigation of mechanisms and possible therapeutic interventions. There are four hypotheses to be tested: 1. Spinal cord injury produces chronic pain which can be measured as alterations in evoked behaviors. 2. Excitatory amino acids (EAA) and peptides play important roles in the alterations of evoked somatosensory behavior observed after spinal cord hemisection. 3. EAAs and peptides play an important role in central sensitization of dorsal horn neurons in nociceptive pathways in this SCI model. 4. Spinal cord injury produces chronic pain which can be measured as alterations in spontaneous, non-evoked behavior. Methods include behavioral tests, electrophysiological recordings, microdialysis and behavioral outcome of pharmacological intervention. These data will contribute toward understanding the symptomology and behavioral changes characteristic of partially spinalized patients.

Project Start
Project End
Budget Start
Budget End
Support Year
22
Fiscal Year
1996
Total Cost
Indirect Cost
Hammell, D C; Zhang, L P; Ma, F et al. (2016) Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis. Eur J Pain 20:936-48
Young, E E; Bryant, C D; Lee, S E et al. (2016) Systems genetic and pharmacological analysis identifies candidate genes underlying mechanosensation in the von Frey test. Genes Brain Behav 15:604-15
Carter, Michael W; Johnson, Kathia M; Lee, Jun Yeon et al. (2016) Comparison of Mechanical Allodynia and Recovery of Locomotion and Bladder Function by Different Parameters of Low Thoracic Spinal Contusion Injury in Rats. Korean J Pain 29:86-95
Yuan, Su-Bo; Ji, Guangchen; Li, Bei et al. (2015) A Wnt5a signaling pathway in the pathogenesis of HIV-1 gp120-induced pain. Pain 156:1311-9
Ji, Guangchen; Li, Zhen; Neugebauer, Volker (2015) Reactive oxygen species mediate visceral pain-related amygdala plasticity and behaviors. Pain 156:825-36
Neugebauer, Volker (2015) Amygdala pain mechanisms. Handb Exp Pharmacol 227:261-84
Hassler, Shayne N; Johnson, Kathia M; Hulsebosch, Claire E (2014) Reactive oxygen species and lipid peroxidation inhibitors reduce mechanical sensitivity in a chronic neuropathic pain model of spinal cord injury in rats. J Neurochem 131:413-7
Ji, Guangchen; Neugebauer, Volker (2014) CB1 augments mGluR5 function in medial prefrontal cortical neurons to inhibit amygdala hyperactivity in an arthritis pain model. Eur J Neurosci 39:455-66
Medina, Georgina; Ji, Guangchen; Grégoire, Stéphanie et al. (2014) Nasal application of neuropeptide S inhibits arthritis pain-related behaviors through an action in the amygdala. Mol Pain 10:32
Kiritoshi, Takaki; Sun, Hao; Ren, Wenjie et al. (2013) Modulation of pyramidal cell output in the medial prefrontal cortex by mGluR5 interacting with CB1. Neuropharmacology 66:170-8

Showing the most recent 10 out of 585 publications