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Neurally mediated effects of metoclopramide on pigeon oesophageal muscle

G La Rocca1, R Fileccia, F Mule

  • 1Dipartimento di Biologia Cellulare e dello Sviluppo, Università di Palermo, Italy.

The Italian Journal of Gastroenterology
|May 1, 1992
PubMed

Insights

Metoclopramide (MCP) excites pigeon esophagus muscles by increasing spike burst frequency. This effect involves cholinergic, non-cholinergic, non-adrenergic neurons, and potentially serotonergic and opioid pathways.

Area of Science:

  • Pharmacology
  • Neuroscience
  • Gastroenterology

Background:

  • Metoclopramide (MCP) is a drug with prokinetic effects.
  • Its precise mechanisms in the esophageal smooth muscle are not fully elucidated.

Purpose of the Study:

  • To investigate the neural mechanisms underlying the excitatory effects of metoclopramide (MCP) in the pigeon esophagus.

Main Methods:

  • In vitro electrophysiological recordings from pigeon esophageal muscular strips.
  • Concentration-response studies with MCP.
  • Pharmacological antagonism using tetrodotoxin, atropine, naloxone, guanethidine, and 5-hydroxytryptamine (5-HT) desensitization.

Main Results:

  • MCP induced a concentration-dependent increase in EMG activity, primarily affecting spike burst frequency.
  • The excitatory effect was blocked by tetrodotoxin, indicating neural mediation.
  • Atropine, naloxone, and 5-HT desensitization partially antagonized the response.
  • Combined naloxone and atropine showed greater antagonism than individual agents.

Conclusions:

  • Metoclopramide (MCP) exerts excitatory effects on pigeon esophagus via neural pathways.
  • These pathways include cholinergic, non-cholinergic, and non-adrenergic neurons.
  • Serotonergic and opioid systems may also contribute to MCP's actions.

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