title: Transient spinal cord ischemia in rat: the time course of spinal FOS protein expression and the effect of intraischemic hypothermia (27 degrees C).
abstract: 1. In the present study, we characterize the time course of spinal FOS protein expression after transient noninjurious (6-min) or injurious (12-min) spinal ischemia induced by inflation of a balloon catheter placed into the descending thoracic aorta. In addition, this work examined the effects of spinal hypothermia on FOS expression induced either by ischemia or by potassium-evoked depolarization (intrathecal KCl). 2. Short-lasting (6-min) spinal ischemia evoked a transient FOS protein expression. The peak expression was seen 2 hr after reperfusion in all laminar levels in lumbosacral segments. At 4 hr of reperfusion, more selective FOS expression in spinal interneurons localized in the central part of laminae V-VII was seen. At 24 hr no significant increase in FOS protein was detected. 3. After 12 min of ischemia and 2 hr of reflow, nonspecific FOS expression was seen in both white and gray matter, predominantly in nonneuronal elements. Intrathecal KCl-induced FOS expression in spinal neurons in the dorsal horn and in the intermediate zone. Spinal hypothermia (27 degrees C) significantly suppressed FOS expression after 6 or 12 min of ischemia but not after KCl-evoked depolarization. 4. Data from the present study show that an injurious (but not noninjurious) interval of spinal ischemia evokes spinal FOS protein expression in glial cells 2 hr after reflow. The lack of neuronal FOS expression corresponds with extensive neuronal degeneration seen in this region 24 hr after reflow. Noninjurious (6-min) ischemia induced a transient, but typically neuronal FOS expression. The significant blocking effect of hypothermia (27 degrees C) on the FOS induction after ischemia but not after potassium-evoked depolarization also suggests that simple neuronal depolarization is a key trigger in FOS induction.
authors.affiliation: Department of Anesthesiology, Chang Gung Memorial Hospital, Niao Shung Hsiang, Kaohsiung Hsien, Taiwan, ROC.
authors.forename: L C
authors.initials: LC
authors.lastname: Yang
authors.forename: J
authors.initials: J
authors.lastname: Orendacova
authors.forename: V
authors.initials: V
authors.lastname: Wang
authors.forename: T
authors.initials: T
authors.lastname: Ishikawa
authors.forename: T L
authors.initials: TL
authors.lastname: Yaksh
authors.forename: M
authors.initials: M
authors.lastname: Marsala
mesh_terms: D000818:Animals; D002404:Catheterization; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D007036:Hypothermia, Induced; D007278:Injections, Spinal; D008297:Male; D010264:Paraplegia / Q000503:physiopathology / Q000628:therapy; D011188:Potassium / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000098:blood supply* / Q000503:physiopathology*; D020760:Spinal Cord Ischemia / Q000503:physiopathology* / Q000628:therapy; D013268:Stimulation, Chemical
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D011188:Potassium