Acetylcholine Synthesis and Glucose Oxidation with Various Oxygen Levels in vivo and in vitro

Abstract

Normal brain function is dependent upon a continual supply of oxygen. For example, memory and the ability to learn a complex task are impaired when the arterial oxygen tension (PaO₂) is reduced from a normal of approximately 90 mm Hg to about 60 mm Hg (13). The biochemical basis of the brain’s sensitivity to a decrease in oxygen (hypoxic hypoxia) is unknown, but it is apparently not due to an inability to maintain the level of energy metabolites (5,14). Consequently, the focus in the search for the molecular mechanism in hypoxia has shifted to those neurotransmitters whose synthesis depends upon oxygen. The rate-limiting step in the formation of dopamine, norepinephrine and serotonin requires molecular oxygen; furthermore, their turnover is decreased by hypoxia. However, the importance of decreased catecholamine and serotonin synthesis in the development of symptoms of hypoxia remains questionable since the turnover of these neurotransmitters is not reduced when hypoxia is accompanied by stress (2).