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Brain Res. 1994 Jan 21;634(2):245-56.

Hippocampal kindling protects several structures from the neuronal damage resulting from kainic acid-induced status epilepticus.

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Department of Psychology, Carleton University, Ottawa, Ont., Canada.


In an attempt to study the effects of piriform cortex damage on kindled seizure propagation, we administered kainic acid (12 mg/kg; i.p.) to rats previously kindled from the dorsal hippocampus. Unexpectedly, the ensuing status epilepticus (SE) in the kindled rats did not result in the piriform cortex damage normally observed in naive rats. As a result of this surprising finding, a more comprehensive investigation was undertaken to compare dorsal hippocampal kindled and control rats on their electrographic and behavioral SE development and subsequent brain damage. The SE induction profile and the pattern of brain damage observed in our control rats was similar to previous reports [Neuroscience, 14 (1985) 375-403; Brain Res., 218 (1981) 299-318]. By contrast, although fewer kindled rats than controls responded to the initial dose of kainic acid with electrographic and behavioral seizures, those many kindled rats that did respond, showed a pattern of SE induction that was different from controls. Kindled rats manifested fewer 'wet dog shakes', more generalized convulsions and a faster development of severe limbic status (SLS) than controls. In addition, without pharmacological intervention, the SLS continued longer in kindled rats than in controls. Histological examination revealed brain damage in kindled rats that was markedly different from controls. Unlike controls, kindled rats had no damage in the piriform cortex or substantia nigra reticulata and minimal hippocampal damage, yet showed midline thalamic and anterior olfactory nuclei damage similar to controls. These differences were observed from 1 to 28 days after kindling. Although the mechanism(s) of this kindling-based neuroprotection is not known, its discovery should add importantly to our understanding of epilepsy-induced alterations of subsequent neuronal function.

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