Comparison of responses to CAP in nodose ganglion neurons from <i>SD rat</i>, <i>BalbC mouse</i>, and <i>C57BL/6 mouse</i>. A)

<p>CAP induces dose dependent increases in cytosolic calcium concentrations in a subpopulation of vagal afferents (black). Some neurons are resistant to CAP even at the highest concentrations tested, but increase calcium following depolarization indicating normal cell viability (gray). Traces are from representative neurons taken from a <i>SD rat</i>. <b>B</b>) High concentrations of CAP increased both the peak and integrated calcium responses. Traces are averages ± SEM across responsive neurons from <i>SD rat</i> (n = 22). <b>C</b>) CAP dose response relationships across species: <i>C57BL/6 mouse</i>, n = 8, EC₅₀ = 10 ± 2 nM CAP, slope = 2.09 ± 0.53, max = 371 ± 89 nM calcium; <i>BalbC mouse</i>, n = 4, EC₅₀ = 54 ± 26 nM CAP, slope = 1.59 ± 0.70 max = 283 ± 179 nM calcium; and <i>SD rat</i>, n = 22, EC₅₀ = 42 ± 6 nM CAP, slope = 2.21 ± 0.29, max = 225 ± 15 nM calcium. Peak calcium influx was not significantly different between groups (ANOVA, P = 0.84); however, the EC₅₀ was lower in neurons from <i>C57BL/6</i> mice compared to both <i>SD</i> rat and <i>BalbC</i> mice due to larger calcium responses at the 10 nM (P < 0.001) and 30 nM (P < 0.001) CAP concentrations. <b>D</b>) Percent of neurons responsive to CAP (100 nM) relative to all HiK responsive neurons within an isolation (<i>SD rat</i>, 80 ± 6%, combined n = 51/63; <i>BalbC</i>, 46 ± 10%, combined n = 38/82; <i>C57BL/6</i>, 64 ± 1%, combined n = 27/42). Both strains of mice had lower percentages of CAP responsive afferents; with the <i>BalbC</i> (Holm-Sidak post-hoc test, P = 0.009), but not the <i>C57BL/6</i> (Holm-Sidak post-hoc test, P = 0.40) afferents statistically lower compared to those taken from the <i>SD</i> rat.