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% CO(2)) evoked a significant release of ACh above the basic spontaneous level, from the medullary and cortical areas. Hypercapnia + hypoxia (12% CO(2) + 8% O(2)), in combination, produced an ACh release comparable to hypercapnia; hypoxia (8% O(2)) had no effect in any region.2. Areas in the medullary reticular formation responsive to injections of CO(2)-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.