Abstract
Serotonin has been implicated in the pathobiology of central nervous system trauma. Using micro-dialysis 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°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°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 patho-physiology of TBI.
Key words:
traumatic brain injury, serotonin, microdialysis
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