Serotonin Augments Gut Pacemaker Activity Figure 5. MEA measurements of ICC electrical activity in the presence of nifedipine (1 mM) and TTX (250 nM). A-B) Field potential images constructed at 200 ms. The top and bottom of the images correspond to the oral and anal ends of the preparation, respectively. C-D) Representative field potential recordings at three channels in the same preparation. The dotted lines indicate the period of the potential images (PI) acquired. E-F) Power spectra constructed from field potential recordings at all 64 channels. A, C and E: control; B, D and F: during application of 5-HT. doi:10.1371/journal.pone.0024928.g005 in ICC, while Ca2+ influx from the extracellular space is required to maintain this [Ca2+]i activity (periodic Ca2+ release) [13], although co-ordinating mechanisms for these Ca2+ pathways are not yet understood. Since 5-HT3 receptors are ligand-gated non- selective cation channels, permeable to Ca2+ [39,40], this channel is likely to act as a Ca2+ influx pathway to enhance pacemaker activity in ICC (Figure S4). This notion is supported by the fact that SK&F96365, which is known to block a broad range of Ca2+- permeable non-selective cation channels [41–43], terminates ICC pacemaker Ca2+ activity even in the presence of 2-Me-5-HT (Fig. 2D). Also, ICC is known to express DHP-insensitive voltage- gated Ca2+-permeable channels [44,45]. This transmembrane PLoS ONE | www.plosone.org 7 September 2011 | Volume 6 | Issue 9 | e24928