SEVERAL studies have demonstrated the ability of experimentally induced seizures to increase the penetration of a variety of blood borne solutes into brain.¹⁻⁵In general, this increase has been attributed to an alteration in the permeability of the blood-brain barrier, as indicated by the increased passage of albumin from blood to central nervous system (CNS).²,³,⁶Under normal conditions, little, if any, blood protein gains access to the CNS.⁷A recent report from this laboratory has shown that the increase in brain permeability to albumin labeled with iodine 131, associated with prolonged pentylentetrazol seizures, was predominantly restricted to the thalamus, reversible within minutes after arrest of the seizure, and accompanied by an appreciable increase in the total water content of the thalamus.⁸These features provided a useful model to assess the effectiveness of glucosteroids on altered brain permeability, since the alteration (1) has a specific localization,
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Eisenberg et al. (1970) studied this question.
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