title: Properties of gastric smooth muscles obtained from mice which lack inositol trisphosphate receptor.
abstract: Membrane potential recordings, made from the circular smooth muscle layer of the gastric antrum taken from mutant mice which lacked the inositol trisphosphate (InsP3) type 1 receptor, were compared with those obtained from the stomach of control (wild-type) mice. Immunostaining of gastric muscles indicated that the distribution and form of c-kit positive cells were similar in wild-type and mutant mice. Smooth muscles from wild-type mice generated slow waves that in turn initiated spike potentials, while those from mutant mice were either quiescent or generated irregular bursts of spike potentials. In the presence of nifedipine, slow waves with reduced amplitude were generated in wild-type mice, while all electrical activity was abolished in mutant mice. Acetylcholine depolarized and sodium nitroprusside hyperpolarized the membrane in muscles from both types of mice, being more effective in wild-type mice. Noradrenaline produced similar hyperpolarizations in both types of mice. Transmural nerve stimulation evoked inhibitory junction potentials (IJPs) in both wild-type and mutant mice. In wild-type mice, the IJPs were reduced in amplitude by nitroarginine and converted to a cholinergic excitatory junction potential (EJP) by apamin. In mutant mice, the IJPs were unaffected by nitroarginine or atropine but were abolished by apamin. It is concluded that in antral smooth muscle, the expression of InsP3 type 1 receptors may be causally related to the generation of slow waves but not to the generation of action potentials. A lack of InsP3 receptors attenuates cholinergic excitatory and nitrergic inhibitory responses but does not alter the response to noradrenaline.
authors.affiliation: Department of Physiology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan. hisuzuki@med.nagoya-cu.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Takano
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Komuro
authors.forename: M
authors.initials: M
authors.lastname: Saito
authors.forename: K
authors.initials: K
authors.lastname: Kato
authors.forename: K
authors.initials: K
authors.lastname: Mikoshiba
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D015220:Calcium Channels / Q000172:deficiency* / Q000235:genetics; D004558:Electric Stimulation; D007150:Immunohistochemistry; D053496:Inositol 1,4,5-Trisphosphate Receptors; D008564:Membrane Potentials; D051379:Mice; D018345:Mice, Knockout; D009130:Muscle, Smooth / Q000187:drug effects* / Q000502:physiology; D009543:Nifedipine / Q000494:pharmacology; D019335:Nitroarginine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D011706:Pyloric Antrum / Q000187:drug effects / Q000502:physiology; D018160:Receptors, Cytoplasmic and Nuclear / Q000172:deficiency* / Q000235:genetics
chemical_list: D015220:Calcium Channels; D053496:Inositol 1,4,5-Trisphosphate Receptors; D018160:Receptors, Cytoplasmic and Nuclear; D019335:Nitroarginine; D001030:Apamin; D019009:Proto-Oncogene Proteins c-kit; D009543:Nifedipine; D000109:Acetylcholine; D009638:Norepinephrine