Studies on the Electrical Stimulation-Induced Contractile Responses of Hamster and Mouse Gallbladders.

Yoshida, Masahide; Koeda, Takemi

doi:10.1540/jsmr.28.111

Cited by 5 publications

(3 citation statements)

References 10 publications

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“…LED illumination of gallbladders from these ChAT-ChR2-tdTomato mice evoked no contraction (fig. S4C), corroborating earlier reports that nerve stimulation does not evoke cholinergic contraction in the mouse gallbladder ( 17 ). In LED-illuminated ChAT-ChR2-EYFP gallbladders, neither the peak response nor the plateau was sensitive to the muscarinic blocker atropine, except when enzymatic ACh breakdown was prevented by the cholinesterase inhibitor eserine (fig.…”

Section: Resultssupporting

confidence: 91%

Cysteinyl leukotrienes and acetylcholine are biliary tuft cell cotransmitters

et al. 2022

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The gallbladder stores bile between meals and empties into the duodenum upon demand and is thereby exposed to the intestinal microbiome. This exposure raises the need for antimicrobial factors, among them, mucins produced by cholangiocytes, the dominant epithelial cell type in the gallbladder. The role of the much less frequent biliary tuft cells is still unknown. We here show that propionate, a major metabolite of intestinal bacteria, activates tuft cells via the short-chain free fatty acid receptor 2 and downstream signaling involving the cation channel transient receptor potential cation channel subfamily M member 5. This results in corelease of acetylcholine and cysteinyl leukotrienes from tuft cells and evokes synergistic paracrine effects upon the epithelium and the gallbladder smooth muscle, respectively. Acetylcholine triggers mucin release from cholangiocytes, an epithelial defense mechanism, through the muscarinic acetylcholine receptor M3. Cysteinyl leukotrienes cause gallbladder contraction through their cognate receptor CysLTR1, prompting emptying and closing. Our results establish gallbladder tuft cells as sensors of the microbial metabolite propionate, initiating dichotomous innate defense mechanisms through simultaneous release of acetylcholine and cysteinyl leukotrienes.

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Section: Resultssupporting

confidence: 91%

Cysteinyl leukotrienes and acetylcholine are biliary tuft cell cotransmitters

et al. 2022

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“…Arachidonic acid (AA) produces contraction of the guinea pig gallbladder in vitro that was blocked by indomethacin, a potent inhibitor of prostanglandins [91,92]. Arachidonic acid (AA) produces contraction of the guinea pig gallbladder in vitro that was blocked by indomethacin, a potent inhibitor of prostanglandins [91,92].…”

Section: )mentioning

confidence: 99%

Anatomy and Physiology of the Biliary Tree and Gallbladder

Toouli¹,

Bhandari²

2006

Diseases of the Gallbladder and Bile Ducts

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“…Observations from studies of intramural nerves in the gallbladder of frogs, toads, hamsters, and mice are inconsistent. According to Yoshida and Koeda (1991, 1992, 1998), the subserosal plexus and perivascular nerves in the gallbladders of frogs, hamsters, and mice are aganglionic. The gallbladder of the bullfrog does not contain intrinsic nerves, motility is not modulated by extrinsic nerves, and spontaneous motility in the gallbladders of hamster and mouse is myogenic in origin.…”

Section: Neuroanatomy Of Gallbladder So and Bile Ductsmentioning

confidence: 99%

Innervation of the extrahepatic biliary tract

2004

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The extrahepatic biliary tract is innervated by dense networks of extrinsic and intrinsic nerves that regulates smooth muscle tone and epithelial cell function of extrahepatic biliary tree. Although these ganglia are derived from the same set of precursor neural crest cells that colonize the gut, they exhibit structural, neurochemical, and physiological characteristics that are distinct from the neurons of the enteric nervous system. Gallbladder neurons are relatively inexcitable, and their output is driven by vagal inputs and modulated by hormones, peptides released from sensory fibers, and inflammatory mediators. Gallbladder neurons are cholinergic and they can express a number of other neural active compounds, including substance P, galanin, nitric oxide, and vasoactive intestinal peptide. Sphincter of Oddi (SO) ganglia, which are connected to ganglia of the duodenum, appear to be comprised of distinct populations of excitatory and inhibitory neurons, based on their expression of choline acetyltransferase and substance P or nitric oxide synthase, respectively. While SO neurons likely receive vagal input and their activity is modulated by release of neuropeptides from sensory fibers, a significant source of excitatory synaptic input to these cells arise from the duodenum. This duodenum-SO circuit is likely to play an important role in the coordination of SO tone with gallbladder motility in the process of gallbladder emptying. Now that we have gained a relatively thorough understanding of the innervation of the biliary tree under healthy conditions, the way is paved for future studies of altered neural function in biliary disease.

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Studies on the Electrical Stimulation-Induced Contractile Responses of Hamster and Mouse Gallbladders.

Abstract: Isolated gallbladders of both hamsters and mice showed a contractile response consist-

Cited by 5 publications

References 10 publications

Cysteinyl leukotrienes and acetylcholine are biliary tuft cell cotransmitters

Cysteinyl leukotrienes and acetylcholine are biliary tuft cell cotransmitters

Anatomy and Physiology of the Biliary Tree and Gallbladder

Innervation of the extrahepatic biliary tract

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