Stimulation by nicotine of enteric inhibitory nerves and release of vasoactive intestinal peptide in the taenia of the guinea-pig caecum

Iselin, Christophe; Martin, Jean‐Luc; Magistretti, Pierre J.; Ferrero, J

doi:10.1016/0014-2999(88)90562-6

Cited by 16 publications

(12 citation statements)

References 25 publications

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“…Many neurotransmitters including substance P and vasoactive intestinal peptide are proposed to be involved in the contractile response in the mouse distal colon (36 -38). Nicotine-induced relaxation seemed to be due to the release of vasoactive intestinal peptiderelated peptides in the guinea-pig caecum (39) and cat esophageal sphincter (40). In preliminary experiments, nicotine-induced relaxation appeared to be partially (approximately 30%) inhibited in the distal colon treated with 1 μM phentolamine.…”

Section: Conclusion and Future Problemsmentioning

confidence: 89%

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

et al. 2009

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Abstract. Nicotine has been shown to reduce both tone and muscular activity in the human colon by releasing nitric oxide (NO) from nerves. To our knowledge, however, the effect of nicotine on mouse colon has not been elucidated, and the response in tissue from ulcerative colitis (UC) has not been investigated. We examined nicotine-induced responses in colon from control mice and mice with dextran sodium sulfate (DSS)-induced UC. In controls, bath application of nicotine caused a transient relaxation in longitudinal preparations from the transverse and distal colons but not from the rectum. The response was observed in the presence of bethanechol, abolished by treatment with tetrodotoxin and hexamethonium, and mediated partially (>50%) by the NO pathway. In longitudinal preparations of the distal colon from DSStreated mice, spontaneous contractions decreased markedly, and nicotine caused contraction without relaxation in half of the preparations tested. Nicotine-induced relaxation in the presence of bethanechol was significantly decreased in the DSS-treated distal colon without changing bethanechol-induced contractions. These data suggest that 1) responses to nicotine differ dependent on colon regions, 2) DSS treatment predominantly caused nicotine-sensitive neurogenic changes in distal colon, and 3) DSS treatment may reverse the direction of nicotine-evoked responses in the colon, in mice.

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Section: Conclusion and Future Problemsmentioning

confidence: 89%

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

et al. 2009

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“…Despite many studies, the identity of the inhibitory neurotransmitter(s) in this tissue has been elusive. Among candidates that have been considered are ATP (Burnstock et al, 1970) and vasoactive intestinal polypeptide (VIP) (Fahrenkrug, 1979;Furness et al, 1981;Iselin et al, 1988) but contradictory evidence concerning these agents has also been presented (Mackenzie & Burnstock, 1980;Westfall et al, 1982). Motoneurones of the guinea-pig taenia coli contain NOS-like immunoreactivity, and these neurones co-express VIP-like immunoreactivity (Furness et al, 1992).…”

Section: Effect Of Oxyhaemoglobin On Neurogenic Relaxations and Membrmentioning

confidence: 99%

Hyperpolarization and inhibition of contraction mediated by nitric oxide released from enteric inhibitory neurones in guinea‐ pig taenia coli

Ward

Dalziel²,

Khoyi³

et al. 1996

British J Pharmacology

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“…It has been suggested that there is a purinergic inhibitory innervation in the guinea-pig taenia caeci (Burnstock et al 1970;Mackenzie & Burnstock, 1980;Satchell, 1981) but there is * To whom correspondence should be addressed. 3581 also evidence that vasoactive intestinal polypeptide (VIP) (Fahrenkrug, 1979;Furness, Costa & Walsh, 1981;Iselin et al 1988), nitric oxide (NO) (Knudsen & T0ttrup, 1992;Poitrowski, Simon & Brennan, 1993) and more recently, pituitary adenylyl cyclase activating peptide (PACAP) (Jin, Katsoulis, Schmidt & Grider, 1994;McConalogue et at. 1995) are inhibitory neurotransmitters.…”

mentioning

confidence: 99%

“…A bewildering number of putative neurotransmitter candidates have been proposed, using immunohistochemical, electrophysiological and mechanical techniques (Bennett, Burnstock & Holman, 1966;Campbell, 1966;Burnstock, Campbell, Satchell & Smythe, 1970;Cocks & Burnstock, 1979;Satchell, 1981;Costa, Furness & Humphreys, 1986;Iselin, Martin, Magistretti & Ferrero, 1988;Furness, Pompolo, Shuttleworth & Burleigh, 1992;Knudsen & T0ttrup, 1992;McConalogue, Furness, Vremec, Holst, Torn0e & Marley, 1995). It is clear that there is a cholinergic excitatory (Bennett, 1966;Campbell, 1966) and a noradrenergic inhibitory innervation.…”

mentioning

confidence: 99%

Characteristic features of inhibitory junction potentials evoked by single stimuli in the guinea‐pig isolated taenia caeci.

Bridgewater

Cunnane

Brading

1995

The Journal of Physiology

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1. Changes in membrane potential of the guinea‐pig isolated taenia caeci evoked by single stimuli have been investigated using intracellular recording techniques. Nifedipine (10 microM) was used to arrest spontaneous muscle action potentials. Single stimuli elicited complex junction potentials which consisted of both excitatory and inhibitory components. 2. The excitatory component of the compound junction potential was unaffected by hexamethonium (100 microM) but abolished by atropine (1 microM) and omega‐conotoxin GVIA (10‐100 nM). 3. In the presence of atropine, single stimuli elicited fast inhibitory junction potentials (IJPs). IJPs were sometimes biphasic during repolarization with a noticeable ‘slow tail’. Apamin (30‐100 nM) potently inhibited the fast IJP and revealed an underlying slow IJP. 4. The fast IJP was also abolished by omega‐conotoxin GVIA (100 nM). However, the slow IJP was insensitive to omega‐conotoxin GVIA but was abolished by cadmium (30 microM). 5. Guanethidine (3 microM) and N omega‐nitro‐L‐arginine (10‐100 microM) had no detectable effects on either of the IJPs. The dye Reactive Blue 2 reduced the amplitude of the fast IJP but this reduction was associated with a membrane hyperpolarization. 6. The existence of two distinct IJPs in the guinea‐pig taenia caeci has been demonstrated. The ability of omega‐conotoxin GVIA to selectively abolish the fast IJP leaving the slow IJP intact suggests that separate nerves are involved in mediating these responses.

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Stimulation by nicotine of enteric inhibitory nerves and release of vasoactive intestinal peptide in the taenia of the guinea-pig caecum

Cited by 16 publications

References 25 publications

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

Hyperpolarization and inhibition of contraction mediated by nitric oxide released from enteric inhibitory neurones in guinea‐ pig taenia coli

Characteristic features of inhibitory junction potentials evoked by single stimuli in the guinea‐pig isolated taenia caeci.

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