SUMMARY The Mg+ + requiring adenosine triphosphatase (ATPase) associated with neuronal synaptic vesicles is extremely vulnerable to ischemia. After five minutes of ischemia both the maximum velocity and the substrate binding capacity of the enzyme were decreased. Results also indicate that these changes are related to the rapid intraneuronal lactic acidosis accompanying ischemia. Ischemia was simulated by 37°C incubation of gerbil brain after decapitation. According to a recent hypothesis this enzyme plays a key role in exocytotic neurotransmitter release. Therefore, any inhibition of the ability of this enzyme to function would result in a drastically reduced capacity for transsynaptic impulse propagation-
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