The role of Ca2+ in cellular injury has received particular attention in studies of acute spinal cord trauma. In this context, the spatial and temporal distribution of extracellular Ca2+ ([Ca2+]e) may have an important bearing on the development of secondary tissue injury. We therefore studied the spatial-temporal distribution of [Ca2+]e following moderate (25 g-cm) contusive injury to the rat thoracic (T9-T11) spinal cord. Double-barreled, Ca(2+)-selective microelectrodes were used to measure the magnitude and time course of [Ca2+]e at increasing depths from the dorsal spinal cord surface. After 2 h, the tissue was frozen and later analyzed for total Ca concentration using atomic absorption spectroscopy. [Ca2+]e fell at all depths, but the decrease was maximal at 250 and 500 microns from the dorsal surface, where, at 0-10 min after injury, [Ca2+]e averaged 0.09 +/- 0.03 and 0.06 +/- 0.03 mM respectively. By 2 h postinjury, [Ca2+]e recovered to nearly 1 mM across all depths. Over this time, total tissue calcium concentration ([Ca]t) was 4.54 +/- 0.16 mumol/g in injured cords vs 2.75 +/- 0.1 mumol/g in sham-operated controls. These data place emphasis on the dorsal gray matter as a principal site of ionic derangement in acute spinal cord injury. The implications of these findings are discussed with reference to secondary injury processes.