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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Neuropharmacology. 2017 Feb 22;117:292–304. doi: 10.1016/j.neuropharm.2017.02.019

Fig. 10.

Fig. 10

TSP4’s regulation of depolarization-induced Ca2+ transient is PKC-dependent. The recovery τ is prolonged and the effect of TSP4 is eliminated by PKC inhibitors GF 109203X (GF, 5 μM) and Calphostin C (CALP, 500nM) in both normal bath solution (A, left) and after isolating SERCA function by bath pH 8.8 (B, left) in small-sized DRG neurons. The PKC activator (PMA, 1 μM) enhances transient recovery and eliminates the effect of TSP4 in both normal bath solution (A, right) and after isolating SERCA function by bath pH 8.8 (B, right). PKA blockers H89 (10 μM) and KT5720 (1 μM) had no effect on TSP4 in both normal bath solution (C) or after isolating SERCA function by bath pH 8.8 (D) in small-sized DRG neurons. * p < 0.05, ** p < 0.01, *** p < 0.001.