EXTRACELLULAR RELEASE OF SEROTONIN FOLLOWING FLUID-PERCUSSION BRAIN INJURY IN RATS

Serotonin has been implicated in the pathobiology of central nervous s ystem trauma. Using microdialysis techniques, we performed measurement s of extracellular serotonin release within the traumatized cerebral c ortex of rats subjected to moderate fluid-percussion (F-P) brain injur y. Twenty-four hours prior to TBI, a F-P interface was positioned para sagitally over the right cerebral cortex. On the second day, fasted ra ts were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxy gen. 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) w ere treated in an identical manner. Brain trauma induced acute elevati ons in the extracellular levels of serotonin (p < 0.01, ANOVA) compare d to sham-operated controls. For example, serotonin levels increased f rom 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 rema ined significantly higher than control for the first 90-min sampling p eriod. In parallel to the increase in serotonin levels after TBI, a si gnificant 71.1% decrease (i.e., 182.29 +/- 30.08 vs 52.75 +/- 16.92) i n extracellular 5-hydroxyindoleacetic acid (5-HIAA) levels was observe d during the first 10 min after TBI. These data indicate that TBI is f ollowed by a prompt increase in the extracellular levels of serotonin in cortical regions adjacent to the impact site. These neurochemical f indings indicate that serotonin may play a significant role in the pat hophysiology of TBI.