Biomedical Engineering Reference
In-Depth Information
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Fig. 12.10  Chemical pain sensor. a Plausible mechanism for the response of a chemical-pain
sensor. After the injection of chemical stimuli, rTRPV1 protein captured the chemical stimuli mol-
ecules and induced the influx of cations, resulting in the conductance decrease of the CNT network
channel. b Real-time conductance measurement data obtained from chemical pain sensors after the
introduction of capsaicin. The conductance decreased after the introduction of capsaicin solution
with picomolar concentration. c Real-time conductance measurement data obtained from chemi-
cal pain sensors after the injection of different chemical stimuli. d Dose-dependent responses of
chemical pain sensors to resiniferatoxin and capsaicin. (Adapted with permission of Jin et al. [ 39 ])
lized chemical pain sensory nanovesicles containing a receptor protein (rTRPV1)
for the detection of chemical pain stimuli. When a CNT-FET functionalized with
rTRPV1-expressed-nanovesicles was exposed to chemical pain stimuli such as
capsaicin and resiniferatoxin, the rTRPV1 on the nanovesicles captures the stimuli
molecules, which eventually induced the influx of cations such as Ca 2+ and Na + into
the nanovesicles through the rTRPV1 [ 40 ]. The increased concentration of positive
ions inside the nanovesicles could give a field effect on the underlying CNT-FET,
resulting in the decrease of a channel conductance because CNTs exhibit p-type
behaviors under ambient conditions.
The injection of capsaicin solutions with concentrations higher than 1 pM in-
duced a change in the conductance of the CNT channel (Fig. 12.10b ). This result
indicates the chemical pain sensor can respond to capsaicin in real time with a high
sensitivity.
 
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