Muscarinic Modulation of Acetylcholine Release from the Myenteric Plexus of the Guinea Pig Small Intestine

  • H. Kilbinger
Part of the Advances in Behavioral Biology book series (ABBI, volume 24)


The concept of a local feedback regulation of neurotransmitter release has been most intensively studied in the adrenergic system (See Ref. 13 for review). The feedback hypothesis of noradrenaline release is based on the findings that α-adrenolytic drugs enhance, and α-adrenoceptor agonists reduce neuronal noradrenaline release. Relatively few systematic studies have been made on the influence of cholinolytic and cholinomimetic drugs on the release of ACh. Szerb and Somogyi (14) reported that the potent muscarinic agonist oxotremorine inhibited ACh output from cerebral cortical slices. Further, the muscarinic antagonists atropine and hyoscine have been found to facilitate the release of ACh from brain tissue in vivo (See Ref. 6 for references) and in vitro (2, 12). These findings led to the hypothesis that there is local regulation of ACh release from central cholinergic neurons via a negative feedback mechanism (12). The aim of the present work was to investigate whether the ACh output from the myenteric plexus of the guinea pig small intestine can also be modulated by atropine and muscarinic drugs.


Myenteric Plexus Acetylcholine Release Negative Feedback Mechanism Stimulation Period Tyrode Solution 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Birks, R. and MacIntosh, F. C. (1961): Canad. J. Biochem. Physiol. 39:787–827.CrossRefGoogle Scholar
  2. 2.
    Bourdois, P.S., Mitchell, J. F., Somogyi, G. T. and Szerb, J. C. (1974): Brit. J. Pharmacol. 52:509–517.Google Scholar
  3. 3.
    Collier, B. and Katz, H.S. (1970): Brit. J. Pharmacol. 39:428–438.Google Scholar
  4. 4.
    Collier, B. and Katz, H.S. (1975): Brit. J. Pharmacol. 55:189–197.Google Scholar
  5. 5.
    Cowie, A.L., Kosterlitz, H.W. and Watt, A.J. (1968): Nature 220:1040–1042.PubMedCrossRefGoogle Scholar
  6. 6.
    Jones, B.E., Guyenet, P., Cheramy, A., Gauchy, C. and Glowinski, J. (1973): Brain Res. 64:355–369.PubMedCrossRefGoogle Scholar
  7. 7.
    Kilbinger, H. and Wagner, P. (1975): N.-S. Arch. Pharmacol. 287:47–60.CrossRefGoogle Scholar
  8. 8.
    Knoll, J. and Vizi, E. S. (1971): Brit. J. Pharmacol. 41:263–272.Google Scholar
  9. 9.
    McKinstry, D.N. and Koelle, G.B. (1967): J. Pharmacol. Exp. Ther. 157:319–327.PubMedGoogle Scholar
  10. 10.
    Paton, W.D. M. and Vizi, E.S. (1969): Brit. J. Pharmacol. 35:10–28.Google Scholar
  11. 11.
    Paton, W.D. M. and Zar, M. A. (1968): J. Physiol. (Lond.) 194:13–33.Google Scholar
  12. 12.
    Polak, R.L. (1971): Brit. J. Pharmacol. 41:600–606.Google Scholar
  13. 13.
    Starke, K. and Endo, T. (1976): Gen. Pharmacol. 7:307–312.PubMedCrossRefGoogle Scholar
  14. 14.
    Szerb, J. C. and Somogyi, G.T. (1973): Nature 241:121–122.Google Scholar
  15. 15.
    Vizi, E.S. (1974): J. Neural Transmission, Suppl. 11:61–78.Google Scholar

Copyright information

© Plenum Press, New York 1978

Authors and Affiliations

  • H. Kilbinger
    • 1
  1. 1.Pharmacology InstituteUniversity of MainzMainzGermany

Personalised recommendations