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A Mapping Study of Caspase-3 Activation Following Acute Spinal Cord Contusion in Rats

Melanie L. McEwen and Joe E. Springer

Department of Physical Medicine and Rehabilitation, University of Kentucky Medical Center, Spinal Cord and Brain Injury Research Center, and Cardinal Hill Rehabilitation Hospital, Lexington, Kentucky

Correspondence to: Melanie L. McEwen, Ph.D., Department of Physical Medicine and Rehabilitation, University of Kentucky Medical Center, Cardinal Hill Rehabilitation Hospital, 800 Rose St., MN 225, Lexington, KY 40536-0298. E-mail: mlmcew2{at}uky.edu

Spinal cord injury (SCI) initiates a cascade of biochemical changes that results in necrotic and apoptotic cell death. There is evidence that caspase-3 activation and apoptotic cell death occur within hours after SCI. However, the time course and cellular localization of activated caspase-3 has not been examined. Such information is essential because caspase-3–independent apoptotic pathways do exist. In this experiment, we describe the distribution of and cell types containing activated caspase-3 at 4 hr, 1 day, 2 days, 4 days, and 8 days following SCI in rats. Numerous caspase-3–positive cells were observed at 4 hr and 1 day postinjury and colocalized most often with CC1, a marker for oligodendroglia. Both markers disappeared near the injury epicenter over the next several days. Activated caspase-3 was again present in the injured spinal cord on postoperative day 8, which coincided with a reemergence of CC1-positive cells. Many of these CC1-positive cells again colocalized activated caspase-3. NeuN-positive neurons of the dorsal horn were occasionally immunopositive for activated caspase-3 at early time points. OX42-positive microglia/macrophages rarely contained activated caspase-3. The results indicate a biphasic pattern of caspase-3 activation during the first 8 days postinjury, suggesting that at least two mechanisms activate caspase-3 following SCI. This time-course study provides a framework for investigating and understanding the different signaling events contributing to this biphasic pattern of caspase-3 activation. (J Histochem Cytochem 53:809–819, 2005)

Key Words: apoptosis • contusion • myelin • secondary injury • spinal cord injury • central nervous system trauma

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