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. Author manuscript; available in PMC: 2012 Oct 1.
Published in final edited form as: Neurobiol Aging. 2009 Dec 1;32(10):1818–1826. doi: 10.1016/j.neurobiolaging.2009.10.017

FIG. 2.

FIG. 2

RACK1 is involved in muscarinic regulation of sIPSC amplitude. A–C, Cumulative plots of the distribution of sIPSC amplitudes (A) and inter-event interval (B), and representative sIPSC traces (C) in a cultured cortical neuron before (ctl) and after carbachol (CCh, 20 μM) application. D–F, Cumulative plots of the distribution of sIPSC amplitudes (D) and inter-event interval (E), and representative sIPSC traces (F) showing the effect of carbachol in a cultured cortical neuron dialyzed with a RACK1 peptide (40 μM). Scale bars: 30 pA, 1s. G,H, Cumulative data (mean ± SEM) showing the percent increase of sIPSC amplitude (G) or frequency (H) by carbachol in the absence or presence of RACK1 peptide, a scrambled control peptide (40 μM), acetylcholinesterase (AChE) inhibitor physostigmine (40 μM), protein phosphatase inhibitor okadaic acid (OA, 1 μM), or PKA inhibitor H89 (10 μM). *: p < 0.01, ANOVA, compared to the effect of carbachol in the control condition (−).