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Figure 7 | Molecular Pain

Figure 7

From: Painful nerve injury increases plasma membrane Ca2+-ATPase activity in axotomized sensory neurons

Figure 7

Regulation of neuronal excitability by PMCA. The afterhyperpolarization (AHP) that follows a train (50 Hz for 4 s) of action potentials (APs) generated by current injection (2x threshold) in control neurons are shown in sample traces (A) made by whole-cell patch-clamp recording 10 min after breakthrough, comparing a recording without vanadate to one in which the patch pipette contained vanadate (200 μM). The traces are aligned at their resting membrane potentials (RMP; -61 mV for the control neuron, -64 mV for the vanadate-treated neuron). The train of APs appears as a black band at the beginning of the trace with their amplitude truncated. Summary data (B) show that the duration of the AHP, measured as the time constant (τ) of a monoexponential fitted to the AHP, was prolonged by vanadate (Van) compared to other neurons without vanadate (w/out Van). The ability to generate APs was tested by determining the ability of a train (50 Hz for 2 s, total 100) of depolarizing stimuli (1.5x threshold) to generate APs. Sample traces in control neurons (C) show 49 full APs produced in a neuron without vanadate and 35 APs produced by comparable stimuli in a vanadate-treated neuron. Summary data (D) reveal a depression of AP generation by PMCA blockade with vanadate in control neurons. In neurons from the fifth lumbar dorsal root ganglia after spinal nerve ligation (SNL L5), sample traces (E) and summary data (F) show that the injury-induced difference in excitability is eliminated by vanadate treatment. Mean ± SD; numbers in bars indicate n; * P < 0.05, *** P < 0.001 by Mann Whitney test.

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