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

In the present study, we characterize the time course of spinal FOS protein expression after transient noninjurious (6-min) or injurious (12-min)spina l ischemia induced by inflation of a balloon catheter placed into the desce nding thoracic aorta. In addition, this work examined the effects of spinal hypothermia on FOS expression induced either by ischemia or by potassium-e voked depolarization (intrathecal KCl). Short-lasting (6-min) spinal ischemia evoked a transient FOS protein expres sion. The peak expression was seen 2 hr after reperfusion in all laminar le vels in lumbosacral segments. At 4 hr of reperfusion, more selective FOS ex pression 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. 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 hor n and in the intermediate zone. Spinal hypothermia (27 degrees C) significa ntly suppressed FOS expression after 6 or 12 min of ischemia but not after KCl-evoked depolarization. Data from the present study show that an injurious (but not noninjurious) i nterval of spinal ischemia evokes spinal FOS protein expression in glial ce lls 2 hr after reflow. The lack of neuronal FOS expression corresponds with extensive neuronal degeneration seen in this region 24 hr after reflow. No ninjurious (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 depolari zation also suggests that simple neuronal depolarization is a key trigger i n FOS induction.