title: Pacemaker phase shift in the absence of neural activity in guinea-pig stomach: a microelectrode array study.
abstract: 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 microm 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 Ca(2+) 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.
authors.affiliation: Department of Cell Physiology, Nagoya University Graduate School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550, Japan. h44673a@nucc.cc.nagoya-u.ac.jp
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Nakayama
authors.forename: Ken
authors.initials: K
authors.lastname: Shimono
authors.forename: Hong-Nian
authors.initials: HN
authors.lastname: Liu
authors.forename: Hideyasu
authors.initials: H
authors.lastname: Jiko
authors.forename: Noburu
authors.initials: N
authors.lastname: Katayama
authors.forename: Tadao
authors.initials: T
authors.lastname: Tomita
authors.forename: Kazunori
authors.initials: K
authors.lastname: Goto
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001683:Biological Clocks / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D004594:Electrophysiology; D005753:Gastric Mucosa / Q000378:metabolism; D005769:Gastrointestinal Motility / Q000187:drug effects / Q000502:physiology*; D006168:Guinea Pigs; D008839:Microelectrodes; D009473:Neuronal Plasticity / Q000502:physiology; D009543:Nifedipine / Q000494:pharmacology; D011042:Poisons / Q000494:pharmacology; D013270:Stomach / Q000166:cytology / Q000294:innervation* / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D011042:Poisons; D013779:Tetrodotoxin; D009543:Nifedipine; D002118:Calcium