Transient spinal cord ischemia in rat: the time course of spinal FOS protein expression and the effect of intraischemic hypothermia (27 degrees C)

• Published in: Cellular and molecular neurobiology Vol. 20; no. 3; pp. 351 - 366
• Main Authors: Yang, L C, Orendacova, J, Wang, V, Ishikawa, T, Yaksh, T L, Marsala, M
• Format: Journal Article
• Language: English
• Published: United States 01.06.2000
• Subjects: Animals; Catheterization; Evoked Potentials - drug effects; Evoked Potentials - physiology; Hypothermia, Induced; Injections, Spinal; Male; Paraplegia - physiopathology; Paraplegia - therapy; Potassium - pharmacology; Proto-Oncogene Proteins c-fos - analysis; Proto-Oncogene Proteins c-fos - biosynthesis; Rats; Rats, Sprague-Dawley; Spinal Cord - blood supply; Spinal Cord - physiopathology; Spinal Cord Ischemia - physiopathology; Spinal Cord Ischemia - therapy; Stimulation, Chemical
• ISSN: 0272-4340
• DOI: 10.1023/A:1007066210294

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.