Intestinal nerves and ion transport: stimuli, reflexes, and responses

Hubel, Kenneth A.

doi:10.1152/ajpgi.1985.248.3.g261

Cited by 57 publications

(39 citation statements)

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“…Sensory mechanism of short-chain fatty acid stimulation Luminal SCFA stimuli are likely to be received at the epithelial sensory receptor cell (Hubel, 1985), not directly at the sensory ending of the secretory nerve reflex or cholinergic nerve terminals, since the serosal application of SCFAs did not elicit an increase in IS., This agrees with previous studies, in which SCFAs did not directly stimulate cholinergic motoneurones or cholinergic nerve terminals in the myenteric plexues of the rat colon (Yajima, 1985). Short-chain fatty acids have no direct effect on the giant nerve fibre of the crayfish abdomen or rat vagal nerves (Hiji, Miyoshi, Ichikawa, Kasagi & Imoto, 1987).…”

Section: Secretory Reflexmentioning

confidence: 99%

Luminal propionate‐induced secretory response in the rat distal colon in vitro.

Yajima

1988

The Journal of Physiology

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SUMMARY1. The stimulatory action of propionate on colonic electrolyte transport and involvement of the enteric reflex in this was studied in vitro using an Ussing chamber in the rat. The short-circuit current (I.,) and bidirectional fluxes of Na+ and Cl-were measured. Mucosa-submucosa preparations, containing the submucosal nerve, from the distal colon were used in most cases.2. Mucosal application of propionate caused transient increases in the transmural potential difference, with the mucosal side negative, ISc and conductance. Serosal application of the acid had no effect.3. Adaptation of the ISC response occurred when the acid was applied to the bathing solution cumulatively without washing out the first dose. If tissues were washed and held more than 20 min before the next application, the response was almost completely restored.4. The increase in IS. in response to propionate was concentration dependent, with a 50% effective concentration of approximately 7 x 10-5 M.5. Two other short-chain fatty acids (SCFAs), n-butyrate and n-valerate, but not acetate, increased ISC when added to the mucosal bathing solution.6. Bumetanide (3 x 10-5 M) and the serosal chloride-free condition, but not amiloride (10-M), inhibited the responses of ISC to propionate. Propionatestimulated Cl-secretion resulted mainly from an increase in unidirectional serosalto-mucosal C1-movement. Propionate did not affect the Na+ flux.7. Tetrodotoxin (10-7 M), somatostatin (10-7 M) and hexamethonium (10-4 M) inhibited the propionate-evoked increase in ISC by 40, 70 and 30°%, respectively.8. Atropine (10-5 M) also inhibited the I,,-increase response to propionate more than 90 %.9. Pre-treatment (2 min) of the mucosal surface with procaine (5 x 10-M)inhibited the propionate-evoked increase in IS. by 90°%.10. The results suggest that luminal propionate transiently stimulated the colonic chloride secretory response that is not due to direct action on colonocytes, but due in large part to release of acetylcholine at neuro-colonocyte junctions, probably via an enteric reflex involving a mucosal sensory mechanism, cholinergic motor nerves and submucosal ganglia.

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Section: Secretory Reflexmentioning

confidence: 99%

Luminal propionate‐induced secretory response in the rat distal colon in vitro.

Yajima

1988

The Journal of Physiology

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“…Given that much of the morbidity associated with inflammatory bowel disease is caused by disordered gastrointestinal motor function and that colonic smooth muscle function is regulated by the ENS, it is quite possible that alterations in the excitability of the enteric neurons contribute to intestinal dysmotility. A variety of immune-mediated inflammatory disorders exist, including Crohn's disease and ulcerative colitis, and dysmotility, hypersecretion, and enhanced perception of pain are common features (17,22,23,46). It is now clear that cutaneous and visceral inflammations lead to enhanced excitability of extrinsic primary afferent neurons and altered reflex activity (5,8,14,48).…”

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confidence: 99%

Effects of PGE₂ in guinea pig colonic myenteric ganglia

Manning

Sharkey

Mawe

2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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is a proinflammatory mediator that can influence many cell types. This study was conducted to determine whether PGE2 alters the electrical activity of distal colonic myenteric neurons, because colitis is typically associated with altered motility and changes in neural signaling may be involved. The electrical properties of intact myenteric neurons were evaluated with intracellular microelectrodes. Acute application of PGE 2 elicited a prolonged depolarization in both AH and S neurons with little effect on input resistance or electrical excitability. PGE 2 effects were suppressed by tetrodotoxin (TTX) or neurokinin (NK) receptor antagonists, indicating that PGE 2 acts directly and indirectly to depolarize colonic neurons. PGE 2-evoked depolarization was concentration dependent (ϳ3 M EC 50) and was attenuated by the E prostanoid (EP)1/2 receptor antagonist, AH-6809. When preparations were maintained for 48 h in the presence of the stable PGE 2 analog PGE2-ethanolamide (10 M), neurons exhibited a significant membrane depolarization and enhanced excitability. These results suggest that PGE 2 can play a role in altered motility in colitis by evoking changes in the electrical properties of myenteric neurons. motility; inflammation; colitis; innervation; enteric nervous system THE NERVOUS SYSTEM OF THE bowel, which is known as the enteric nervous system (ENS) regulates visceromotor, secretomotor, and vasomotor activities in the wall of the intestines. Given that much of the morbidity associated with inflammatory bowel disease is caused by disordered gastrointestinal motor function and that colonic smooth muscle function is regulated by the ENS, it is quite possible that alterations in the excitability of the enteric neurons contribute to intestinal dysmotility. A variety of immune-mediated inflammatory disorders exist, including Crohn's disease and ulcerative colitis, and dysmotility, hypersecretion, and enhanced perception of pain are common features (17,22,23,46). It is now clear that cutaneous and visceral inflammations lead to enhanced excitability of extrinsic primary afferent neurons and altered reflex activity (5,8,14,48). Changes may also occur in the afferent components of intrinsic enteric neural circuitry, and such changes could contribute to altered motor reflex activity in the inflamed bowel.In guinea pig bowel, it is possible to identify the functional role of a given neuron on the basis of consensus knowledge regarding the electrical, morphological, chemical coding, and axonal projection patterns of these cells. For example, a class of cells known as AH neurons, on the basis of electrical properties, functions as the afferent limb of the peristaltic reflex circuit (19) and is considered to have roles as intrinsic primary afferent neurons and interneurons (for review, see Ref. 30). These cells have a Dogiel type II morphology (multiple processes) and extend projections to other ganglia and to the lamina propria (7,34,40,42), where they could respond to stimuli originating at the mucosal surface. Therefor...

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“…This leads to two actions of the adrenergic agonist epinephrine : a direct action on the enterocyte that stimulates electrolyte absorption and an indirect action on submucosal neurons that inhibits the release, from intramural nerves, of neurotransmitters which have a secretory effect on the enterocytes (Hubel, 1976(Hubel, , 1985Cooke, 1986 ;Keast et al, 1986). In the present experiment the 6-CM analog effect was entirely inhibited by epinephrine, whereas epinephrine effect was only partially (50 %) reduced by the peptide.…”

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confidence: 55%