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. Author manuscript; available in PMC: 2011 Jul 1.
Published in final edited form as: J Neurochem. 2010 Apr 29;114(2):430–439. doi: 10.1111/j.1471-4159.2010.06779.x

Figure 6.

Figure 6

Evidence that S1P generation is sufficient and necessary for the increased neuronal excitability resulting from nSMase activation. A. S1P increases action potential firing frequency in CA1 pyramidal neurons. Upper panel): Representative traces generated from a single 50 pA depolarizing step measured 15 minutes after establishing whole cell condition in the absence (control) and presence (S1P) of S1P in the intracellular pipette. Lower panel): Cumulative data (bottom panel) showed a significant difference in the firing frequency between control (n = 8) and S1P-treated (n = 8) neurons. B. nSMase-mediated increase in action potential firing is attenuated by sphingosine-kinase inhibition. Action potential firing under perforated patch condition was increased following nSMase exposure (15 min; 0.4 U/ml) compared to baseline (n = 10). Incubation of slices with the sphingosine kinase inhibitor N,N-DMS (10 uM) for 30 – 90 min prior to nSMase application (15 min; 0.4 U/ml, n = 5) blocked the increase in action potential firing. Data are presented as the mean ± SEM. Student’s t-test was used for statistical comparisons. *p < 0.05.