Figure 2.

Response of cytoplasmic Ca²⁺ concentration ([Ca²⁺]_c) in sensory neurons to application of caffeine (20mM) during pharmacological blockade of processes that extrude and sequester Ca²⁺. A. Typical traces of caffeine-induced Ca²⁺ release in the presence of the mitochondrial protonophore p-trifluoromethoxy carbonyl cyanide phenyl hydrazone (FCCP), which eliminates buffering of cytoplasmic Ca²⁺ by mitochondria, and increases amplitude of the transient while eliminating the plateau phase. B. Spinal nerve ligation (SNL) depresses the amplitude of caffeine-induced transients during FCCP in the axotomized neurons of the fifth lumbar (L5) dorsal root ganglion. C. Typical traces of caffeine-induced Ca²⁺ transients in the presence of FCCP, and thapsigargin (TG), which blocks sequestration of Ca²⁺ by the sarcoplasmic/endoplasmic reticulum Ca²⁺ ATPase (SERCA), as well as La³⁺, which blocks extrusion of Ca²⁺ from the neuron by the plasma membrane Ca²⁺ ATPase (PMCA) and the Na⁺/Ca²⁺ exchanger. D. SNL depresses amplitude of the resulting caffeine-induced transient in the L5 population. For panels B and D, one-way ANOVA with Bonferroni post-hoc testing was used, numbers in the bars indicate n for number of neurons, and brackets above bars connect groups that are significantly different (P<0.05), and error bars show standard deviation.