Ecto-ATPase deficiency in glia of seizure-prone mice

Abstract

A DEFICIENCY of calcium-stimulated adenosine triphosphatase (Ca²⁺-ATPase) is seen in brains of mice which are susceptible to audiogenic seizures¹. After studying five other animal models of idiopathic epilepsy we concluded that brain nucleotide metabolism is altered in the epileptic animals and that the lesion might not be confined to Ca²⁺-ATPase². We speculated that the deficiency of Ca²⁺-ATPase, which we observed in membrane-enriched brain homogenates, was the expression of incompetent brain cell ecto-ATPases. We have suggested that the genesis of seizures was related to a protracted action of translocated cytoplasmic ATP on cell membranes³ when the latter were deficient in this enzyme. We report here a significant deletion of ecto-ATPase in cultured glia cells raised from neonatal, seizure-prone mice. Between the ages of 20 to 35 d, mice of the DBA/2N strain convulse after repeated exposure to loud noise. Before and after this period, susceptibility to induced convulsions is minimal or absent. Mice of the C57 B1/6N strain are not afflicted in this manner.