Correlation between the Electrical Activity and Acetylcholine Release from the Cerebral Cortex and Medulla during Hypercapnia

Abstract

Studies were undertaken to determine whether any correlation exists between the level of acetylcholine (ACh) release from the cerebral cortex and medulla and the electrical activity within those same brain areas during hypercapnia, hypoxia, and hypoxia plus hypercapnia in combination. The cerebral cortex and medulla of anesthetized dogs released ACh spontaneously through push–pull cannulae after perfusion with an anticholinesterase, sarin. Hypercapnia (12% CO2) evoked an increased release of ACh above the basic spontaneous level from the cerebral cortex and medulla, with a parallel rise in the integrated electrical activity as monitored by EEG recordings. Hypoxia plus hypercapnia (8% O2 + 12% CO2) induced an ACh release comparable with hypercapnia alone, but with no change in the electrical activity. Hypoxia (8% O2) produced no increase in ACh release or electrical activity. Areas in the medullary reticular formation responsive to injections of CO2-buffered bicarbonate solutions ("respiratory responsive areas") produced during hypercapnia an augmented release of ACh, paralleled by a concomitant rise in the electrical activity, both of which were of greater magnitude than that manifested in either the "nonrespiratory responsive areas" of the medulla or in the cerebral cortex. The data suggest that a correlation exists between the ACh release and the electrical activity during hypercapnia. Thus, cholinergic neurons in the cerebral cortex and medulla may be activated during hypercapnia and are possibly involved in the medullary regulation of respiration. Furthermore, the evidence supports the concept that the pathways involved in EEG activation and ACh release are distinct.