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. 2012 Apr 13;7(4):e34755. doi: 10.1371/journal.pone.0034755

Figure 3. Cholecystokinin (CCK) produces nearly identical activation of cultured vagal afferents from the rat and mouse species. A).

Figure 3

CCK produces dose dependent increases in cytosolic calcium concentrations in a subpopulation of vagal afferents. Neurons were also challenged with CAP to determine afferent subtype and HiK to verify viability (data not shown). Trace is from a representative neuron taken from a C57BL/6 mouse. B) CCK dose response relationships across species/strains: C57BL/6 mouse, n  =  4, EC50  =  0.60 ± 0.22 nM CCK, slope  =  1.24 ± 0.26, max  =  108 ± 23 nM calcium; BalbC mouse, n  =  5, EC50  =  0.92 ± 0.77 nM CCK, slope  =  3.03 ± 29.5, max  =  99 ± 31 nM calcium; and SD rat, n  =  7, EC50  =  0.95 ± 0.35 nM CCK, slope  =  1.58 ± 0.40, max  =  77 ± 10 nM calcium. C) Percent of total viable neurons tested responsive to CCK. Results from challenges with 10 nM CCK were used to determine population characteristics (SD rat, 45 ± 5%, combined n  =  35/75; BalbC, 33 ± 6%, combined n  =  41/111; C57BL/6, 40 ± 2%, combined n  =  38/90). D) Percent of CCK responsive neurons also activated by CAP (SD rat, 67 ± 9%, combined n  =  15/21; BalbC, 90 ± 6%, combined n  =  17/19; C57BL/6, 69 ± 3%, combined n  =  13/19).