*2.6. Modulation of Evoked EPSCs by AITC in the Caudal NTS*

AITC significantly modulated evoked EPSCs generated by electrical stimulation of the solitary tract (50–400 μs, pulse duration; 100–500 μA, pulse intensity; 60 s inter-pulse interval). The average amplitude of EPSCs was 131.86 pA ± 41.29 (*n* = 14) (ranged between 40.00 pA to 396.19 pA) and AITC (100 μM) failed to alter the EPSC amplitude or kinetics (*p* > 0.05; *n* = 14, Figure 9A,C). In experiments where a paired-pulse protocol was employed, AITC significantly depressed the paired-pulse ratio (PPR) in a concentration-dependent manner (control, 0.6877 ± 0.163, *n* = 12; 100 μM, 0.770 ± 0.060, *n* = 10; 200 μM, 0.7 ± 0.086, *n* = 4; 500 μM, 0.517 ± 0.051, *n* = 7, *p* < 0.05; 1 mM, 0.117 ± 0.179, *n* = 8, *p* < 0.05; Figure 9B,D). It is interesting to note that stimulation of TRPV1 significantly inhibited the evoked responses as reported by Peters et al., 2010 [46]. The differential modulation of synaptic transmission by TRPA1 and TRPV1 is intriguing. These results are consistent with the expression of TRPA1 in the primary afferent solitary tract terminals in the caudal NTS.

**Figure 9.** AITC-induced effects on solitary tract-evoked synaptic responses in horizontal brainstem slices. (**A**,**B**) Representative traces of solitary tract-stimulated EPSCs (ST-EPSCs) showing seven overlapping sweeps. (**A**,**C**) AITC does not have any significant effect on the amplitude of the ST-EPSCs (*n* = 14). (**B**,**E**) AITC depressed the paired pulse ratio (PPR, EPSC2/EPSC1) in a concentration dependent manner. (**D**) AITC does not show any significant effect on the failure rate (% failures = (number of failures/total stimulations) × 100%) in NTS neurons (*n* = 11). The asterisk (\*) represents *p* < 0.05 as compared to control.
