Extracellular release of serotonin following fluid-percussion brain injury in rats

Serotonin has been implicated in the pathobiology of central nervous system trauma. Using microdialysis techniques, we performed measurements of extracellular serotonin release within the traumatized cerebral cortex of rats subjected to moderate fluid-percussion (F-P) brain injury. Twenty-four hours prior to TBI, a F-P interface was positioned parasagitally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5 degrees C), rats were injured (n = 6) with a F-P pulse ranging from 1.8 to 2.0 atm. Following trauma, brain temperature was maintained for 4 h at 37 degrees C. Sham trauma animals (n = 7) were treated in an identical manner. Brain trauma induced acute elevations in the extracellular levels of serotonin (p < 0.01, ANOVA) compared to sham-operated controls. For example, serotonin levels increased from 18.85 +/- 7.12 pm/mL (mean +/- SD) in baseline samples to 65.78 +/- 11.36 in the first 10 min after trauma. The levels of serotonin remained significantly higher than control for the first 90-min sampling period. In parallel to the increase in serotonin levels after TBI, a significant 71.1% decrease (i.e., 182.29 +/- 30.08 vs 52.75 +/- 16.92) in extracellular 5-hydroxyindoleacetic acid (5-HIAA) levels was observed during the first 10 min after TBI. These data indicate that TBI is followed by a prompt increase in the extracellular levels of serotonin in cortical regions adjacent to the impact site. These neurochemical findings indicate that serotonin may play a significant role in the pathophysiology of TBI.