Modulation of cholinergic neurotransmitter release from myenteric plexus by somatostatin

Peptides. 1983 Jan-Feb;4(1):49-53. doi: 10.1016/0196-9781(83)90164-x.


Efflux of radiolabeled acetylcholine (Ach) was studied in vitro using myenteric plexus-longitudinal muscle strips from guinea pig small intestine. The data showed that somatostatin (6.0 x 10(-7) M) depressed resting output of Ach from enteric neurons and this inhibition was unaltered in the presence of naloxone (1.0 x 10(-6) M). The inhibition by somatostatin on field-stimulated Ach release was dose-dependent but this inhibition was never complete; there was a 40% fraction of total release remained resistant to somatostatin. Both caerulein (2.85 x 10(-9) M) and guanidine (3.0 x 10(-3) M) stimulated release of [H3]-Ach from plexus neurons. The release of Ach induced by guanidine or caerulein was also susceptible to inhibition by somatostatin (6.0 x 10(-7) M). This study provides functional evidence to further substantiate an inhibitory action on plexus cholinergic neurons by somatostatin.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetylcholine / metabolism
  • Animals
  • Ceruletide / pharmacology
  • Electric Stimulation
  • Female
  • Guanidine
  • Guanidines / pharmacology
  • Guinea Pigs
  • Myenteric Plexus / drug effects
  • Myenteric Plexus / metabolism*
  • Naloxone / pharmacology
  • Neurotransmitter Agents / metabolism*
  • Parasympathetic Nervous System / drug effects
  • Parasympathetic Nervous System / metabolism*
  • Somatostatin / pharmacology*
  • Time Factors


  • Guanidines
  • Neurotransmitter Agents
  • Naloxone
  • Somatostatin
  • Ceruletide
  • Guanidine
  • Acetylcholine