Spinal cord injury in rats is known to cause anatomical, physiological and molecular changes within the spinal cord. These changes may account for behavioral syndromes that appear following
spinal cord injury, syndromes believed to be related to the clinical condition of
chronic pain.
Intraspinal injection of
quisqualic acid produces an excitotoxic injury with pathological characteristics similar to those associated with ischemic and traumatic
spinal cord injury. In addition, recent studies have demonstrated changes in blood flow, neuronal excitability and gene expression in the brain following excitotoxic injury, indicating that behavioral changes may result from modification of neuronal substrates at supraspinal levels of the neuraxis. Because changes in spinal
opioid peptide expression have been demonstrated in models of traumatic
spinal cord injury and
chronic pain, the present study investigated
messenger RNA expression of the
opioid peptides,
preproenkephalin and
preprodynorphin, at spinal and supraspinal levels following excitotoxic
spinal cord injury. Male, Long-Evans rats were given three
intraspinal injections of
quisqualic acid (total 1.2 microl, 125mM). After one, three, five, seven or 10days, animals were killed and quantitative in situ hybridization performed on regions of the spinal cord surrounding the lesion site, as well as whole-brain sections through various levels of the thalamus.
Preproenkephalin and
preprodynorphin expression was increased in spinal cord areas adjacent to the site of quisqualic injection and in cortical regions associated with nociceptive function,
preproenkephalin in the cingulate cortex and
preprodynorphin in the parietal cortex, both ipsilaterally and contralaterally at various time-points following injury. These results further our knowledge of the secondary events that occur following
spinal cord injury, specifically implicating supraspinal
opioid systems in the CNS response to
spinal cord injury.