Cholinergic contractions induced by GABA-A receptor activation in the guinea-pig ileum are inhibited by α-chymotrypsin and potentiated by diazepam

M. Tonini, L. Onori, L. Manzo, C. A. Rizzi, A. Crema

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The influence of α-chymotrypsin and diazepam on the phasic (mainly direct) and tonic (indirect, probably substance P-mediated) components of intestinal cholinergic contractions, induced by the GABA-A receptor agonist 3-aminopropane sulphonic acid (3-APS), was investigated in the guinea-pig ileum. α-Chymotrypsin, at a concentration (20 U/ml) not affecting submaximal Ach (0.1 μM) contractions, preferentially depressed the tonic component of the 3-APS (30 μM)-induced response. A brief exposure (10 or 60 sec) to diazepam (0.1 μM) potentiated both the phasic and the tonic contractions evoked by low (10, 30 μM) 3-APS concentration. This potentiation was prevented by bicuculline (30 μM), hyoscine (1 μM) and flumazenil (1, 3 μM). These results provide further support for an involvement of a peptide neurotransmitter on GABA-A receptor-mediated cholinergic response in the ileum. The modulation of this response by diazepam is probably exerted through recognition sites resembling the 'central type' benzodiazepine receptors.

Original languageEnglish
Pages (from-to)173-183
Number of pages11
JournalArchives Internationales de Pharmacodynamie et de Therapie
Volume296
Publication statusPublished - 1988

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Sulfonic Acids
Chymotrypsin
GABA-A Receptors
Diazepam
Ileum
Cholinergic Agents
Guinea Pigs
GABA-A Receptor Agonists
Flumazenil
Scopolamine Hydrobromide
Bicuculline
Substance P
Neurotransmitter Agents
Peptides

ASJC Scopus subject areas

  • Pharmacology

Cite this

Cholinergic contractions induced by GABA-A receptor activation in the guinea-pig ileum are inhibited by α-chymotrypsin and potentiated by diazepam. / Tonini, M.; Onori, L.; Manzo, L.; Rizzi, C. A.; Crema, A.

In: Archives Internationales de Pharmacodynamie et de Therapie, Vol. 296, 1988, p. 173-183.

Research output: Contribution to journalArticle

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