In Vivo Effects of Capsazepine on Trigeminal

1
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 alimhx00_at_wfu.
edu, silver_at_wfu.edu
Introduction
Conclusions
Methods
Results
Systemic administration of capsazepine
specifically reduces nasal trigeminal nerve
responses to carbon dioxide. 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. 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 nAChR function, and can be
reliably used as a specific vanilloid receptor
blocker in future in vivo studies.
Figure 5. Differential Effect of Capsazepine
Figure 3. Response to Carbon Dioxide
Figure 1. Experimental Setup
Methods
Figure 4. Response to Nicotine
Figure 6. Response 30 Minutes Post-Treatment
Figure 2. Representative Data
Literature Cited
Carbon Dioxide
Nicotine Vapor
CAPSAZEPINE
CAPSAZEPINE
CONTROL
CONTROL
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
(n5 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.
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 rats 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.