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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.