title: Mechanical responses evoked by nerve stimulation in gastric muscles of mouse lacking inositol trisphosphate receptor.
abstract: Alteration of mechanical responses elicited by transmural nerve stimulation (TNS) was investigated in pylorus muscle of stomach isolated from mutant mice lacking expression of IP, type-1 receptor. In wild and mutant mice. TNS inhibited spontaneous contractions and generated an off-response at the cessation. The effects of inhibitors of neurotransmission revealed that in wild mice, acetylcholine and nitric oxide were involved as excitatory and inhibitory mediators, respectively. In mutant mice, a lack of nitroxidergic component with associated attenuation of cholinergic transmission was found. The off-response was inhibited by apamin in both mice. In mutant mice, spantide-sensitive excitatory response appeared in the presence of apamin. Acetylcholine and substance P enhanced while noradrenaline and sodium nitroprusside inhibited spontaneous contractions, in both wild and mutant mice; the actions were weaker in mutant mice than in wild mice for any agonists. The results indicate that pylorus smooth muscles receive cholinergic excitatory and nitroxidergic and non-adrenergic non-cholinergic inhibitory projections, and a lack of IP, type-1 receptor results in an impairment of cholinergic and nitroxidergic components, with no alteration of non-adrenergic non-cholinergic inhibitory projections. In addition, the mutation induces a substance P projection which is not detected in wild mice.
authors.affiliation: Department of Physiology, Nagoya City University Medical School, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Takano
authors.forename: K
authors.initials: K
authors.lastname: Imaeda
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Kato
authors.forename: K
authors.initials: K
authors.lastname: Mikoshiba
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000700:Analgesics / Q000494:pharmacology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D015220:Calcium Channels / Q000235:genetics*; D002799:Cholinergic Fibers / Q000502:physiology; D004558:Electric Stimulation; D005746:Gastric Emptying / Q000187:drug effects / Q000502:physiology; D053496:Inositol 1,4,5-Trisphosphate Receptors; D051379:Mice; D008817:Mice, Mutant Strains; D009130:Muscle, Smooth / Q000294:innervation* / Q000502:physiology*; D009388:Neostigmine / Q000494:pharmacology; D009433:Neural Inhibition / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine; D010277:Parasympathomimetics / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol; D011708:Pylorus / Q000294:innervation* / Q000502:physiology*; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics*; D013373:Substance P / Q000031:analogs & derivatives / Q000494:pharmacology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D000700:Analgesics; D015220:Calcium Channels; D053496:Inositol 1,4,5-Trisphosphate Receptors; D010277:Parasympathomimetics; D018160:Receptors, Cytoplasmic and Nuclear; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D001030:Apamin; D009569:Nitric Oxide; D013373:Substance P; D009388:Neostigmine; C042867:spantide; D011433:Propranolol; D000109:Acetylcholine; D009638:Norepinephrine; D010646:Phentolamine