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The CogNet Library : References Collection
mitecs_logo  Wasterlain : Table of Contents: Pathophysiology of Seizure Circuitry in Status Epilepticus : Section 1
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The basic model

The model of SE that we describe was based first on the antecedent development of a kindled site in each rat. We originally defined kindling as the progressive and permanent increase in triggered afterdischarge activity and associated behavioral correlates that resulted from discrete, daily electrical stimulation of certain forebrain sites, particularly limbic sites (15). In the majority of kindling studies, most researchers develop their triggered kindled seizures to the level of stage 5, rearing-and-falling convulsive responses (38), and with protracted kindling, spontaneous seizures also begin to appear (31, 37).

A decade or so after presenting the initial kindling studies, we reported that protracted, low-intensity electrical stimulation of a kindled focus would trigger SE in many of the kindled rats, but in only a few of the nonkindled controls (30). The development of SE usually occurred only in rats that expressed numerous (more than six) stage 5 seizures during the 60-minute stimulation procedure. During that same stimulation period, some rats did not develop SE and became relatively refractory to the stimulation, both behaviorally and electrographically. SE did develop in most rats, but it presented in a variety of isoforms. In an individual rat, one isoform ultimately and invariably predominated.

In the model we describe here, rats underwent amygdala kindling to six stage 5 seizures, followed by 3 weeks of rest. To induce SE, they were subsequently reexposed to the kindling stimulus but in a near-continous form for 60 minutes.

 
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