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Background: The cortical spreading depression (CSD) is a phenomenon associated with several pathological conditions including migraine. It can induce alterations in both neural and vascular compartments. Serotonin (5-HT) depletion is known as a condition involved in migraine pathophysiology. The hyper-excitability of the cortical neurons to the CSD activation in the low 5-HT state has been previously reported. However, the cerebrovascular responses to CSD activation in this condition have never been studied yet. Objectives: Determine the effect of 5-HT depletion on the cerebrovascular responses to CSD activation. Methods: Wistar rats (weighing 250-300 grams) were divided into three groups: control, CSD, and low 5-HT with CSD group (five rats per group). To induce the low 5-HT state, the para-chlorophenylalanine was injected intraperitoneally into the rats three days before the experiment. CSD was induced by the application of solid KCl (3 mg) on the parietal cortex. NaCl instead of KCl was applied to the control group. Cerebral cortical blood flow was monitored using Laser Doppler flowmetry. The ultrastructure of cerebral microvessels was examined using electron microscopy to determine the cerebral microcirculatory responses to CSD. Results: Depletion of serotonin induced a significant increase in the peak amplitude of CSD-evoked cerebral hyperaemia. This condition also enhanced the development of CSD-induced endothelial pinocytosis and microvillus formation in cerebrocortical microvessels. Conclusion: 5-HT was an important neurotransmitter involved in the control of cerebrovascular responses to CSD activation. The hypersensitivity of the cerebrovascular responses observed in the 5-HT depleted state may explain the relationship between headache and 5-HT depletion.

Effect of serotonin depletion on cortical spreading depression evoked cerebrovascular changes