A cholinergic mechanism involved in fetal breathing during the high voltage ECoG state

John M. Bissonnette, A. Roger Hohimer, Sharon J. Knopp

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

The effects of muscarininc cholinergic neurotransmission on fetal breathing was determined by administration of carbachol or carbachol plus a muscarinic receptor antagonist into the cerebrospinal fluid of the fourth ventricle in unanesthetized fetal sheep. In the hour following the instillation of carbachol (1.0 μg), the incidence of fetal breathing in high voltage electrocortical state (ECoG) increased to 63 ± 11.7 (SEM) percent compared to 1.2 ± 0.9 after instillation of vehicle (Ringer solution). The cholinergic agonist increased breath amplitude from 4.5 ± 0.4 to 10.6 ± 1.4 mmHg. These effects were eliminated when the M1 receptor antagonist pirenzipine (50-100 μg) was administered with carbachol but not by antagonists which are relatively selective for M2 or M3 receptors. When administered alone, muscarinic receptor antagonists did not effect the incidence or amplitude of fetal breathing in low voltage. These data indicate that the apnea which occurs during high voltage in the sheep fetus involves an inhibition of acetylcholine acting at M1 muscarinic receptor bearing neurons.

Original languageEnglish (US)
Pages (from-to)151-162
Number of pages12
JournalRespiration Physiology
Volume96
Issue number2-3
DOIs
StatePublished - May 1994

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Keywords

  • Fetal breathing sheep, muscarinic effects
  • Mammals, sheep (fetal)
  • Mediators, central, acetylcholine, fetal breathing
  • Sheep, fetal breathing, central mediators
  • control of breathing, sleep, central mediators (fetal sheep)

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine

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