The goal of these studies is to investigate the microcircuitry of the spinal cord dorsal horn to determine the relationship of various spinal cord structures to pain transmission systems. An understanding of spinal cord microcircuitry in the normal animal will allow us to determine if changes have occurred in hyperalgesic states, such as acute inflammation. The descending noradrenergic system is proposed as one route by which the perception of pain is modulated endogenously. Norepinephrine has been shown to selectively inhibit noxious input to spinothalamic tract neurons. We have recently shown in the past grant period that noradrenergic terminals synapse directly on the soma and proximal dendrites of lamina I, IV, and V neurons. This included three retrogradely identified and two intracellularly filled spinothalamic tract neurons. The intracellularly filled neurons were a wide dynamic range neuron and a high threshold neuron. The current proposal outlined here will continue study of the inhibitory noradrenergic system and expand the scope of the grant to study of glutamate and aspartate as examples of candidate excitatory neurotransmitters. Specifically, the dorsal horn will be surveyed to determine what arrangements exist within the normal dorsal horn with identified noradrenergic and then with excitatory amino acid structures. The relationship of noradrenergic and excitatory amino acid structures to spinothalamic tract neurons and their dendrites be examined in detail. It has been reported that glutamate content in primary afferent neurons. If possible, differences between glutamate structures from various sources will be identified. Finally, comparison of normal structure will be made with tissues at three time points after an experimentally induced inflammation of the knee capsule. Increased knowledge of the microcircuitry of inhibitory noradrenergic and excitatory amino acid systems in the normal and in the acute arthritis model may impact on our future effectiveness of pain management.

Project Start
Project End
Budget Start
Budget End
Support Year
21
Fiscal Year
1995
Total Cost
Indirect Cost
Name
University of Texas Medical Br Galveston
Department
Type
DUNS #
041367053
City
Galveston
State
TX
Country
United States
Zip Code
77555
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
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
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; Gr├ęgoire, St├ęphanie 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