Cortical changes in cholecystokinin mRNA are related to spontaneous pain behaviors following excitotoxic spinal cord injury in the rat

Cholecystokinin (CCK) in the CNS antagonizes the opioid system and has been implicated post-spinal cord injury (SCI) pain. The current study found that excitotoxic SCI alters levels of CCK mRNA levels in the cortex, diencepahlon, and mesencephalon of rats. Animals that developed pain post-SCI had si...

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Veröffentlicht in:	Brain research. Molecular brain research. 2003-10, Vol.118 (1), p.171-174
Hauptverfasser:	Brewer, Kori L., McMillan, David, Nolan, Todd, Shum, Kerry
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Behavior, Animal - physiology Biochemistry and metabolism Biological and medical sciences Central nervous system Cerebral Cortex - metabolism Cholecystokinin - genetics Diencephalon - metabolism Disease Models, Animal Efferent Pathways - metabolism Efferent Pathways - physiopathology Excitotoxicity Fundamental and applied biological sciences. Psychology Grooming - physiology Gyrus Cinguli - metabolism Gyrus Cinguli - physiopathology Mesencephalon - metabolism Neuronal Plasticity - genetics Neurons - metabolism Neuropathic pain Opioid Peptides - antagonists & inhibitors Opioid Peptides - metabolism Pain - genetics Pain - metabolism Pain - physiopathology Quisqualic acid Rats RNA, Messenger - metabolism Slot blot Spinal Cord Injuries - genetics Spinal Cord Injuries - metabolism Spinal Cord Injuries - physiopathology Up-Regulation - genetics Vertebrates: nervous system and sense organs
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Zusammenfassung:	Cholecystokinin (CCK) in the CNS antagonizes the opioid system and has been implicated post-spinal cord injury (SCI) pain. The current study found that excitotoxic SCI alters levels of CCK mRNA levels in the cortex, diencepahlon, and mesencephalon of rats. Animals that developed pain post-SCI had significantly higher levels than animals that did not develop pain. Upregulation of CCK mRNA in the cortex may be related to post-SCI pain in rats.
ISSN:	0169-328X 1872-6941
DOI:	10.1016/j.molbrainres.2003.08.006