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. 1966 Oct;186(2):321–332. doi: 10.1113/jphysiol.1966.sp008037

Hypercapnia and acetylcholine release from the cerebral cortex and medulla

B Metz
PMCID: PMC1395848  PMID: 5972111

Abstract

1. The cerebral cortex and medulla of fifty-eight anaesthetized dogs released ACh spontaneously through push-pull cannulae after perfusion with the anticholinesterase, sarin. Hypercapnia (12% CO2) evoked a significant release of ACh above the basic spontaneous level, from the medullary and cortical areas. Hypercapnia + hypoxia (12% CO2 + 8% O2), in combination, produced an ACh release comparable to hypercapnia; hypoxia (8% O2) had no effect in any region.

2. Areas in the medullary reticular formation responsive to injections of CO2-bicarbonate solutions (`respiratory responsive areas') produced a significant increase of ACh after exposure to hypercapnia or hypercapnia + hypoxia, over that obtained from either the `non-respiratory responsive areas' of the medulla or the cerebral cortex.

3. The evidence supports the concept that ACh may participate as a neurotransmitter within the cerebral cortex and medulla. Also the results would suggest but do not prove, that a cholinergic factor may be a component in respiratory control under certain circumstances, such as exposure to hypercapnia.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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