Effect of serotonin depletion and chemically induced facial inflammation on cerebral cortical activity and expression of vanilloid receptor subtype 1 in rat trigeminal system

Abstract

Determines the effect of serotonin (5-HT) depletion and/or facial inflammation on the development of cortical spreading depression (CSD) and trigeminal nociception. Adult male Wistar rats were divided into four groups, including those receiving complete Freund's adjuvant (CFA), receiving para-chlorophenylalanine (PCPA), receiving both CFA and PCPA and control groups. Facial inflammation was induced by subcutaneous injection with CFA in the forehead area. 5-HT was depleted by administration of PCPA (100 mg/kg BW, intraperitoneally), a tryptophan hydroxylase inhibitor. CSD was induced by application of 3 mg of potassium chloride crystal on parietal cortex. Cortical activity was monitored using glass microelectrode inserted into frontal cortex ipsilateral to the potassium chloride application. Impact on trigeminal nociceptive system was studied using the expression of vanilloid receptor (VR1) in trigeminal ganglia as well as the expression of a transcription factor Fos in trigeminal nucleus caudalis as indicators. The results showed that application of potassium chloride resulted in a series of depolarization activity characteristic for CSD. The development of these CSD waves was enhanced in both PCPA-treated and CFA-treated groups. No additional effect was evident when both interventions were combined. Such enhancement was characterized by increased area under the curve of each CSD wave, shortened interpeak latency as well as an increase in frequency of CSD waves. No significant change was observed regarding the peak amplitude and duration. Results from the Fos- and VR1-immunohistochemical studies revealed the similar pattern. Greater numbers of Fos in trigeminal nucleus caudalis and VR1 in trigeminal ganglia were observed in both PCPA- and CFA- treated groups. Again, no addition effect was evidenced. The present study demonstrated the plasticity of trigeminal nociceptive system. Serveral factors, including facial tissue inflammation and 5-HT depletion asshown in the present study, can enhance this system by increasing the cortical response as well as facilitating the trigeminal nociception in general