Autoreceptors regulate γ-[3H]aminobutyric acid release from the guinea pig small intestine

Taniyama, Kohtaro; Hanada, Susumu; Tanaka, Chikako

doi:10.1016/0304-3940(85)90028-x

Cited by 10 publications

(3 citation statements)

References 13 publications

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“…Although the functional role of GABA on intestinal motility is not clear, inhibitory effects of GABA on the release of neurotransmitters from guineapig ileum are well known (Kerr and Ong 1986). GABA inhibits via GABA B receptors the field stimulationevoked release of acetylcholine (Kleinrok and Kilbinger 1983) and via GABA A autoreceptors the release of GABA itself (Taniyama et al 1985). The present study and our previous experiments (Hebeiß and Kilbinger 1999) show that both receptor subtypes affect the synthesis and release of NO from nitrergic neurons.…”

Section: Figsupporting

confidence: 48%

GABAergic inhibition of nitric oxide-mediated relaxation of guinea-pig ileum

Kilbinger

Ginap

Erbelding

1999

Naunyn-Schmiedeberg's Arch Pharmacol

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The effects of GABA receptor agonists were investigated on guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus. Electrical field stimulation (1 Hz, 10 s) of the histamine (1 microM)-precontracted preparation caused a contraction followed by a relaxation. Relaxations were inhibited by L-N(G)-nitroarginine (L-NA; EC50 3 microM) in a concentration-dependent manner. The inhibitory action of 10 microM L-NA was blocked by 10 microM L-arginine but not by D-arginine, which indicates that the relaxation was largely mediated by endogenous nitric oxide (NO). Tetrodotoxin (1 microM) reduced the relaxation only by about 50%. GABA and the GABA(B) agonist, baclofen, inhibited the field stimulation-induced longitudinal muscle relaxation in a concentration-dependent manner. The GABA(B) receptor antagonist, saclofen (10 microM), antagonised the effect of baclofen (apparent pA2 of saclofen: 5.6). Muscimol (10 microM) similarly inhibited the relaxation, and this inhibition was prevented by bicuculline (1 microM). It is concluded that nitrergic nerves of the guinea-pig myenteric plexus are endowed with GABA(A) and GABA(B) receptors which mediate inhibition of NO release.

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Section: Figsupporting

confidence: 48%

GABAergic inhibition of nitric oxide-mediated relaxation of guinea-pig ileum

Kilbinger

Ginap

Erbelding

1999

Naunyn-Schmiedeberg's Arch Pharmacol

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“…At the present time, details of the mechanism of action of these phenomena are not available, but its elucidation is expected to provide an important clue to the explanation of the mechanism of action of the physiological factors participating in cholinergic motor regulation of gastrointestinal motility (Vizi, 1973;Szurszewski, 1976;Pernow, 1983;Yau et al, 1983;Taniyama, 1985;Tanaka et al, 1985;. The contents which accumulated in the Thiry loop, were evacuated by the strong initial contractions appearing in the loop by cisapride administration (Fig.…”

Section: Methodsmentioning

confidence: 99%

“…In recent years, the existence has been reported of various endogenous substances which act either stimulatively (gastrin, CCK, susbtance P, neurotensin, GABA) or inhibitively (noradrenaline, dopamine, enkephalin, VIP), on ACh release (Vizi et al, 1973;Szurszewski, 1976;Pernow, 1983;Yau et al, 1983;Taniyama et al, 1985;Tanaka et al, 1985;.…”

Section: Introductionmentioning

confidence: 99%

Effect of cisapride on the cholinergic control mechanisms of gastrointestinal motility in dogs.

Fujii

Okajima

Kawahori

1988

Jpn. J. Smooth Muscle Res.

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Administration of cisapride in the digestive state resulted in the excitatory response of increased amplitude of digestive peristalsis and strong IMC-like motility was not observed .All of these excitatory responses in gastrointestinal motility disappeared by the administration of atropine (0.05 mg-0.1 mg/kg body weight, i.v.). Furthermore, the excitatory response in gastrointestinal motility induced by cisapride in anesthetized dogs disappeared by the administration of TTX (10 ug/kg of body weight, i.v.).These results suggest that the excitatory action of cisapride on the gastrointestinal motility is based on its mechanism in which cisapride acts on the cholinergic neurones in the gastrointestinal wall to stimulate ACh release, resulting in the increase in gastrointestinal motility.Cisapride caused powerful IMC-like motility in the ileum of animal with pseudoobstruction-like motor disturbance which had been seen after preparation of Thiry loop (ileum). This motility migrated from the proximal ileum to the Thiry loop and then to the distal ileum. Trimebutine maleate also demonstrated this effect, but metoclopramide and domperidone were ineffective.Administration of cisapride at the doses (0.2 mg-1.0 mg/kg body weight , i.v.) causing stimulated motor response in the gastrointestinal tract did not induce significant secretion of gastric acid, pancreatic juice and bile.

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Cellular and Biochemical Responses to GABAB Receptor Activation

Cunningham¹,

Enna²

1997

The GABA Receptors

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Autoreceptors regulate γ-[3H]aminobutyric acid release from the guinea pig small intestine

Cited by 10 publications

References 13 publications

GABAergic inhibition of nitric oxide-mediated relaxation of guinea-pig ileum

GABAergic inhibition of nitric oxide-mediated relaxation of guinea-pig ileum

Effect of cisapride on the cholinergic control mechanisms of gastrointestinal motility in dogs.

Cellular and Biochemical Responses to GABAB Receptor Activation

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