Browse the latest research summaries in the field of pain management for spinal cord injury patients and caregivers.
Showing 671-680 of 682 results
BMC Neuroscience, 2006 • January 12, 2006
The study investigates the expression and function of ZAS3, a zinc finger protein, in the nervous system and its relationship with NF-κB after peripheral nerve injury. Results show that ZAS3 is expres...
KEY FINDING: ZAS3 is expressed in specific regions of the central and peripheral nervous system, including the trigeminal ganglion, hippocampal formation, dorsal root ganglia, and motoneurons.
The Journal of Neuroscience, 2006 • April 19, 2006
This study investigates the role of activated microglia in maintaining chronic pain after spinal cord injury (SCI) in rats. The researchers hypothesized that activated spinal microglia contribute to c...
KEY FINDING: Thoracic spinal cord injury (SCI) in rats causes chronic activation of microglia in the lumbar spinal cord.
Molecular Pain, 2006 • August 17, 2006
This study demonstrates that peripheral nerve injury induces changes in the excitability and sodium channel expression in the VPL nucleus of the thalamus. Specifically, the expression of Nav1.3 sodium...
KEY FINDING: Peripheral nerve injury (CCI) leads to increased firing rates of VPL neurons in response to peripheral stimuli.
The Journal of Neuroscience, 2007 • February 28, 2007
This study demonstrates a PGE2-dependent, ERK1/2-regulated microglia–neuron signaling pathway that mediates the microglial component of pain maintenance after injury to the spinal cord. The researcher...
KEY FINDING: Phosphorylated ERK1/2 (pERK1/2), an upstream regulator of PGE2 release, is specifically localized to microglial cells in the lumbar dorsal horn after SCI.
The Journal of Neuroscience, 2007 • August 15, 2007
This study demonstrates that spinal cord injury (SCI) induces microglial activation in the ventral posterolateral (VPL) nucleus of the thalamus, a brain region involved in pain processing. The chemoki...
KEY FINDING: CCL21 is upregulated in dorsal horn neurons and tissue levels are increased in the dorsal horn and VPL nucleus of the thalamus 4 weeks after SCI.
Nat Neurosci, 2008 • April 1, 2008
Systemic artemin treatment caused the regeneration of damaged axons, resulting in virtually complete and long-lasting restoration of nociceptive and sensorimotor functions. Artemin, given in six syste...
KEY FINDING: Systemic artemin administration promotes the regrowth of both myelinated and unmyelinated axons through the dorsal root entry zone (DREZ).
The Journal of Neuroscience, 2008 • December 3, 2008
The study investigates the role of dendritic spine remodeling in the maintenance of neuropathic pain after spinal cord injury (SCI). SCI leads to altered spine morphologies and distribution in dorsal ...
KEY FINDING: SCI induces dendritic spine remodeling in dorsal horn neurons, characterized by increased spine density, altered spine distribution, and more mature spine morphology.
JOURNAL OF NEUROTRAUMA, 2009 • October 1, 2009
This study evaluated the effect of buprenorphine on molecular, behavioral, electrophysiological, and histological levels after SCI in rats. The rats were injured at the T10 thoracic level and half rec...
KEY FINDING: Microarray analysis showed no significant difference in gene expression between rats treated with buprenorphine and the control group at 2 and 4 days post-injury (DPI).
J Comp Neurol, 2010 • August 1, 2010
This study investigated the impact of peripheral nerve injury on the central projections of DRG neurons expressing GFRs, focusing on GFRα1, GFRα2, and GFRα3 after sciatic nerve injury in rats. The key...
KEY FINDING: Sciatic nerve injury caused a widespread increase in nerve fiber labeling for GFRα1 in the lumbar dorsal horn.
J Pain, 2010 • November 1, 2010
This study demonstrates that skin incision, even without direct nerve injury, induces the expression of axonal regeneration-related genes in adult rat spinal sensory neurons. The researchers observed ...
KEY FINDING: Skin incision led to a significant increase in ATF3 expression in DRG neurons.