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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 576/3/727    most recent jphysiol.2006.118893v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Nakayama, S. Articles by Goto, K. Search for Related Content PubMed PubMed Citation Articles by Nakayama, S. Articles by Goto, K. Related Collections Alimentary

¹ Department of Cell Physiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
² Alpha MED Sciences, Kadoma, Osaka 571-8505, Japan

Gastrointestinal (GI) motility is well organized. GI muscles act as a functional syncytium to achieve physiological functions under the control of neurones and pacemaker cells, which generate basal spontaneous pacemaker electrical activity. To date, it is unclear how spontaneous electrical activities are coupled, especially within a micrometre range. Here, using a microelectrode array, we show a spatio-temporal analysis of GI spontaneous electrical activity. The muscle preparations were isolated from guinea-pig stomach, and fixed in a chamber with an array of 8 x 8 planar multielectrodes (with 300 µm in interpolar distance). The electrical activities (field potentials) were simultaneously recorded through a multichannel amplifier system after high-pass filtering at 0.1 Hz. Dihydropyridine Ca²⁺ channel antagonists are known to differentiate the electrical pacemaker activity of interstitial cells of Cajal (ICCs) by suppressing smooth muscle activity. In the presence of nifedipine, we observed spontaneous electrical activities that were well synchronized over the array area, but had a clear phase shift depending on the distance. The additional application of tetrodotoxin (TTX) had little effect on the properties of the electrical activity. Furthermore, by constructing field potential images, we visualized the synchronization of pacemaker electrical activities resolving phase shifts that were measurable over several hundred micrometres. The results imply a phase modulation mechanism other than neural activity, and we postulate that this mechanism enables smooth GI motility. In addition, some preparations clearly showed plasticity of the pacemaker phase shift.

(Received 9 August 2006; accepted after revision 15 September 2006; first published online 21 September 2006)
Corresponding author S. Nakayama: Department of Cell Physiology, Nagoya University Graduate School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550, Japan.  Email: h44673a{at}nucc.cc.nagoya-u.ac.jp