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. Author manuscript; available in PMC: 2015 Jul 2.
Published in final edited form as: J Pharmacol Sci. 2015 Jan 5;127(1):10–16. doi: 10.1016/j.jphs.2014.12.013

Fig. 3.

Fig. 3

Diagram showing our hypothesis for the role of the S1R in C-terminals: A. The S1R regulates the activity of potassium channels located in postsynaptic sites of C-terminals. In WT animals the S1R will activate potassium channels resulting in a larger afterhyperpolarization that reduces the firing frequency in motoneurons. In sigma-1 KO animals, a reduced afterhyperpolarization results in a higher firing frequency and a stronger muscle contraction. B and C: Two possible mechanisms showing how S1R can regulate the activity of potassium channels in the postsynaptic plasma membrane. B. The enzyme INMT produces the ligand that activates the S1R localized in the subsurface cisternae. Active S1R results in a conductance increase in calcium channels, and the subsequent opening of potassium channels (SK2 and/or Kv2.1) through calmodulin (CaM), leading to an after-hyperpolarization. C. S1R can directly interact with and modulate potassium channels, resulting in an increased conductance of the SK2 and/or Kv2.1 channels in the plasma membrane of C-terminals.