title: Deficiency of intramuscular ICC increases fundic muscle excitability but does not impede nitrergic innervation.
abstract: The motility of the gastrointestinal tract is generated by smooth muscle cells and is controlled to a large extent by an intrinsic neural network. A gap of approximately 200 nm usually separates nerve varicosities from smooth muscle cells, which suggests that direct innervation of the smooth muscle by synapses does not occur. Enteric nerves do make synapse-like contact with proposed regulatory cells, the interstitial cells of Cajal (ICC), which in turn may be in gap junction contact with smooth muscle cells. The role played by ICC in enteric innervation is controversial. Experimental evidence has been presented in vitro for the hypothesis that nitrergic inhibitory innervation is strongly reduced in the absence of ICC. However, in vivo data appear to dispute that. The present report provides evidence that explains the discrepancy between in vivo and in vitro data and provides evidence that inhibitory neurotransmitters can reach smooth muscle cells without hindrance when ICC are absent. The fundic musculature shows increased responses to substance P-mediated innervation and shows marked spontaneous activity, which is consistent with increased muscle excitability.
authors: Intestinal Disease Research Program, Department of Medicine, McMaster University, Hamilton, ON, L8N 3Z5, Canada. huizinga@mcmaster.ca
authors: Jan D
authors: JD
authors: Huizinga
authors: Louis W C
authors: LW
authors: Liu
authors: Amanda
authors: A
authors: Fitzpatrick
authors: Elizabeth
authors: E
authors: White
authors: Sandeep
authors: S
authors: Gill
authors: Xuan-Yu
authors: XY
authors: Wang
authors: Natalia
authors: N
authors: Zarate
authors: Lynn
authors: L
authors: Krebs
authors: Catherine
authors: C
authors: Choi
authors: Tanya
authors: T
authors: Starret
authors: Devika
authors: D
authors: Dixit
authors: Jing
authors: J
authors: Ye
mesh_terms: D018663:Adrenergic Agents / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004558:Electric Stimulation; D017615:Enteric Nervous System / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005748:Gastric Fundus / Q000294:innervation / Q000502:physiology; D006145:Guanethidine / Q000494:pharmacology; D007150:Immunohistochemistry; D051379:Mice; D008854:Microscopy, Electron; D018721:Muscarinic Agonists / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000294:innervation / Q000502:physiology* / Q000648:ultrastructure; D018377:Neurotransmitter Agents / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D051381:Rats; D013270:Stomach / Q000166:cytology* / Q000502:physiology* / Q000648:ultrastructure
chemical_list: D018663:Adrenergic Agents; D004791:Enzyme Inhibitors; D018721:Muscarinic Agonists; D018377:Neurotransmitter Agents; D019335:Nitroarginine; D009569:Nitric Oxide; D001285:Atropine; D019001:Nitric Oxide Synthase; D006145:Guanethidine