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

Ward, Sean M.; Dalziel, H. H.; Khoyi, M. A.; Westfall, Alison S.; Sanders, Kenton M.; Westfall, David P.

doi:10.1111/j.1476-5381.1996.tb15365.x

Cited by 32 publications

(32 citation statements)

References 26 publications

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“…This suggests that endogenous NO, released by field stimulation, decreases the evoked release of acetylcholine from enteric neurones. There are, however, tissue and species differences in the neuromodulatory effect of NO: NO or NOS inhibitors do not modify the electrically evoked acetylcholine release from the colon of guinea pig and dog (22,29) and from stomach preparations of man (13 …”

mentioning

confidence: 99%

Modulation by NO of acetylcholine release in the ileum of wild-type and NOS gene knockout mice

Mang

Truempler

Erbelding

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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Mang, Christian F., Sebastian Truempler, Doris Erbelding, and Heinz Kilbinger. Modulation by NO of acetylcholine release in the ileum of wild-type and NOS gene knockout mice. Am J Physiol Gastrointest Liver Physiol 283: G1132-G1138, 2002 10.1152/ajpgi.00192.2002 inhibits the release of acetylcholine and cholinergic contractions in the small intestine of several species, but no information is available about the mouse ileum. This study examines the effects of NO on the electrically evoked release of 3 H]acetylcholine release and cholinergic contractions in preparations from wild-type mice and from eNOS knockout mice. Effects of L-NNA were specifically antagonized by L-arginine. In contrast, L-NNA and ODQ did not modify the release and contractions in preparations from nNOS knockout mice. The NO donor S-nitroso-N-acetyl-DLpenicillamine inhibited the electrically evoked release of [ 3 H]acetylcholine and longitudinal muscle contractions in a quantitatively similar manner in wild-type preparations as well as in nNOS and eNOS knockout preparations. We conclude that endogenous NO released by electrical field stimulation tonically inhibits the release of acetylcholine. Furthermore, data suggest that nNOS and not eNOS is the enzymatic source of NO-mediating inhibition of cholinergic neurotransmission in mouse ileum. neuronal nitric oxide synthase knockout mice; endothelial nitric oxide synthase knockout mice; cholinergic neurotransmission NITRIC OXIDE (NO) is a nonadrenergic, noncholinergic neurotransmitter that causes inhibition of intestinal motility (for review, see Ref. 24). The relaxant action of NO is probably not confined to its direct action on smooth muscle, because NO decreases intestinal motility also indirectly by inhibiting the release of the functionally most prominent excitatory enteric neurotransmitters acetylcholine and substance P. For example, exogenous NO (31) and NO donors (5) inhibit the electrically evoked release of acetylcholine from guinea pig ileum. Vice versa, NO synthase (NOS) inhibitors enhance the evoked release of acetylcholine from the ileum of guinea pig (10,20) and dog (7) as well as the electrically evoked cholinergic and tachykininergic contractions of guinea pig ileum (6,32). This suggests that endogenous NO, released by field stimulation, decreases the evoked release of acetylcholine from enteric neurones. There are, however, tissue and species differences in the neuromodulatory effect of NO: NO or NOS inhibitors do not modify the electrically evoked acetylcholine release from the colon of guinea pig and dog (22,29) and from stomach preparations of man (13

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mentioning

confidence: 99%

Modulation by NO of acetylcholine release in the ileum of wild-type and NOS gene knockout mice

Mang

Truempler

Erbelding

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…M2rs have also been suggested to modulate pre-and post-synaptic release of other transmitter substances, such as tachykinins, vasoactive intestinal peptide, serotonin and noradrenaline (North et al 1985;Racke et al 1991;Ward et al 1996;Tonini et al 2001). We found M2r-IR present on tachykinergic SP-IR nerve fibres in both the myenteric and submucosal ganglia.…”

Section: Discussionmentioning

confidence: 69%

Immunohistochemical localisation of pre-synaptic muscarinic receptor subtype-2 (M2r) in the enteric nervous system of guinea-pig ileum

2008

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The cholinergic muscarinic 2 receptor (M2r) is known to be present on smooth muscle cells in the intestine. Pharmacological studies also suggest that M2rs regulate transmitter release from nerves in the enteric nervous system. This study localised M2rs in the guinea-pig ileum using different antibodies and fluorescence immunohistochemistry. Double labelling with antibodies against neurochemical markers was used to identify the type of nerves bearing M2r. Guinea-pig ileum were fixed, prepared for sections and wholemounts and incubated with antisera against the M2r sequence. Tissue was double labelled with antibodies against neuronal nitric oxide synthase (nNOS), common choline acetyltransferase (cChAT), substance P (SP), synaptophysin and vesicular acetylcholine transporter (VAChT). Immunofluorescence was viewed using confocal microscopy. Abundant M2r-immunoreactivity (IR) was present on the surface of circular and longitudinal smooth muscle cells. M2r-IR was present in many but not all nerve fibres in the circular muscle and ganglia. M2r-IR was present in VAChT-IR and cChAT-IR cholinergic nerve fibres and SP-IR nerve fibres in the myenteric ganglia and submucosal ganglia. M2r-IR was present on a few nNOS-IR nerve fibres and around nNOS-IR neurons in the myenteric ganglia. In the circular muscle and deep muscular plexus, M2r-IR was present in many VAChT-IR and SP-IR nerve fibres and in few nNOS-IR nerves. M2rs are not only present on muscle cells in the intestine, but also on nerve fibres. M2rs may mediate cholinergic reflexes via their location on muscle and also via neural transmission. The pre-synaptic location supports pharmacological studies suggesting M2rs mediate neurotransmitter release from nerve fibres. The presence of M2rs on VAChT-IR, SP-IR and nNOS-IR-containing nerve fibres suggests M2rs may regulate ACh, SP and nitric oxide release.

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“…Other groups support the view that NO is partially or wholly responsible for NANC inhibitory transmission in both guinea pig (Shuttleworth et al 1991(Shuttleworth et al , 1999Caballero Alomar et al 1999) and human (Tam and Hillier 1992). Other studies, however, argue against NO as an inhibitory transmitter in the taenia coli; one shows that, while NO is released during NANC stimulation, postjunctional effects are not apparent when atropine is present (Ward et al 1996;Selemidis et al 1997). In addition, Selemidis et al (1997), contrary to a previous study, failed to demonstrate any block of NANC relaxations by L-NOARG in the absence of atropine.…”

Section: Caecum and Taenia Colimentioning

confidence: 87%

Peripheral Nervous System

Burnstock¹,

Verkhratsky

2012

Purinergic Signalling and the Nervous System

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

Abstract: 1 Inhibition of nitric oxide synthase by N0-nitro-L-arginine (L-NNA) reduced the neurogenic relaxation of precontracted taenia coli only in the absence of atropine.

Cited by 32 publications

References 26 publications

Modulation by NO of acetylcholine release in the ileum of wild-type and NOS gene knockout mice

Modulation by NO of acetylcholine release in the ileum of wild-type and NOS gene knockout mice

Immunohistochemical localisation of pre-synaptic muscarinic receptor subtype-2 (M2r) in the enteric nervous system of guinea-pig ileum

Peripheral Nervous System

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