In Vivo Effects of Capsazepine on Trigeminal Nerve

In Vivo Effects of Capsazepine on Trigeminal Nerve Sensitivity to Carbon Dioxide and Nicotine Hessamedin Alimohammadi and Wayne L. Silver Department of Biology, Wake Forest University, Winston-Salem, NC 27109 alimhx 00@wfu. edu, silver@wfu. edu Introduction Methods Results Figure 1. Experimental Setup Audio Monitor Amplifier Integrator Circuit Probe Oscilloscope Gnd G 2 Nasopharyngeal tube Data Acquisition System Capsazepine treatment does not completely abolish trigeminal nerve sensitivity to carbon dioxide, suggesting the involvement of more than one receptor mechanism for carbon dioxide. These results suggest that at the concentration tested, systemic CPZ does not interfere with n. ACh. R function, and can be reliably used as a specific vanilloid receptor blocker in future in vivo studies. Trigger Stimulus Marker Tracheal tube Control Figure 4. Response to Nicotine Figure 6. Response 30 Minutes Post-Treatment Capsazepine Neural Response Integrated Response Stimulus Marker Nicotine Vapor Nasal trigeminal nerve response to nicotine is not significantly affected by systemic administration of capsazepine. Significant levels of reduction in the trigeminal nerve response to carbon dioxide are reached within 30 minutes of intraperitoneal injection of capsazepine. Figure 2. Representative Data Carbon Dioxide Figure 5. Differential Effect of Capsazepine Amplifier Olfactometer Methods Figure 3. Response to Carbon Dioxide Systemic administration of capsazepine specifically reduces nasal trigeminal nerve responses to carbon dioxide. Respiration G 1 To Vacuum Conclusions Neural Response Integrated Response CONTROL CAPSAZEPINE Stimulus Marker Figure 1. Experimental setup. Stimuli were presented via a computer-controlled air-dilution olfactometer. Data were recorded using an automated acquisition system controlled by the olfactometer. Respiration was monitored via a thermocouple inserted into the rat’s breathing tube. Figure 2. Representative data showing neural and integrated neural response of the ethmoid nerve to a 5 second presentation of carbon dioxide (50%) or nicotine vapor (12. 5 ppm). Response magnitude was calculated as the amplitude difference between the maximum integrated response value and the mean baseline value 5 -seconds prior to the onset of stimulus delivery. Mean percent response curves showing changes in the magnitude of the ethmoid nerve response to carbon dioxide (Figure 3) and nicotine (Figure 4) over a 10 minute time period (three stimulus presentations). Percent response values were calculated as a percentage of the first response magnitude, which was recorded 20 minutes after administration of either capsazepine or the control solution. Error bars represent one standard deviation unit. Administration of capsazepine resulted in a significant decrease in the ethmoid nerve response to carbon dioxide, whereas response to nicotine remained unchanged (n=5 for all groups). Figure 5. Time course of relative capsazepine effect on carbon dioxide and nicotine. The relative strength of capsazepine effect was calculated as the quotient of the control and capsazepine treated response values at each stimulus presentation (capsazepine efficacy index). The effect of capsazepine on the nerve response to carbon dioxide increased over time. There was no change on the nerve response to nicotine vapor. Figure 6. Trigeminal nerve response to carbon dioxide and nicotine 30 minutes after administration of capsazepine. Response to carbon dioxide is ~50 of the original response, whereas response to nicotine is unchanged. Literature Cited