*2.7. Data from TRPA1 Knockout Mice Support the Modulatory Role of TRPA1 in the Caudal NTS*

TRPA1 knockout mice were used to further elucidate the modulatory role of presynaptic TRPA1 in the caudal NTS. In experiments using brainstem slices from TRPA1 knockout mice, AITC (200 μM) was ineffective in increasing mEPSC frequency (as a percent of control): 105.21 ± 12.23% (*n* = 15, Figure 10A,B,D; vs. effects of AITC in caudal NTS neurons obtained from wild-type mice: 450.63 ± 22.74% (*n* = 13, *p* < 0.05) Figure 2A,B,D). In the same experiments, TRPV1 agonist, capsaicin (100 nM) significantly increased the frequency of mEPSCs (309.88 ± 42.06%, *n* = 7, Figure 10A,B,D). These experiments further confirmed that the observed effects of AITC were mediated by TRPA1.

**Figure 10.** AITC does not induce enhancement of synaptic transmission in the TRPA1 knockout mice. (**A**) Application of AITC (200 μM) does not increases the frequency of mEPSC in the TRPA1 knockout mice (105.21 ± 12.23%, *n* = 15, *p* > 0.05); whereas, capsaicin increase the frequency of mEPSC significantly (309 ± 42%, *n* = 7, *p* < 0.05); The synaptic events are shown in higher time resolution below. (**B**) Cumulative probability plot showing decreased interevent intervals representing increased frequency of mEPSCs mediated by capsaicin (i.e., CAP; *p* < 0.0001, KS test), but no change of interevent intervals mediated by AITC. (**C**) There was no change in the amplitude in all three groups. (**D**) Summary graph showing only capsaicin-mediated increases but no AITC mediated changes in the frequency of mEPSCs (\* *p* < 0.05). The asterisk (\*) represents *p* < 0.05 as compared to control.
