Epileptogenesis and chronic seizures in a mouse model of temporal lobe epilepsy are associated with distinct EEG patterns and selective neurochemical alterations in the contralateral hippocampus

May 19, 2005Experimental neurology

Seizure development and ongoing seizures in a mouse model of temporal lobe epilepsy show unique brain wave patterns and specific chemical changes in the opposite side of the memory area

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Abstract

A significant decrease in theta oscillations was observed bilaterally during the chronic phase of temporal lobe epilepsy in a mouse model.

Unilateral kainic acid injection into the dorsal hippocampus induces a non-convulsive status epilepticus and subsequent neuronal degeneration.
Spontaneous focal seizures appear during the chronic phase, while the contralateral hippocampus remains unaffected.
Bilateral EEG recordings show reduced synchronization of activity during the latent phase, independent of recurrent seizures.
Immunohistochemical analysis reveals reduced calbindin-labeling of CA1 pyramidal cells in the contralateral hippocampus.
Changes in neurochemical markers, such as down-regulation of CCK-8 and up-regulation of NPY, suggest altered neuronal excitability.

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Major aspects of temporal lobe epilepsy (TLE) can be reproduced in mice following a unilateral injection of kainic acid into the dorsal hippocampus. This treatment induces a non-convulsive status epilepticus and acute lesion of CA1, CA3c and hilar neurons, followed by a latent phase with ongoing ipsilateral neuronal degeneration. Spontaneous focal seizures mark the onset of the chronic phase. In striking contrast, the ventral hippocampus and the contralateral side remain structurally unaffected and seizure-free. In this study, functional and neurochemical alterations of the contralateral side were studied to find candidate mechanisms underlying the lack of a mirror focus in this model of TLE. A quantitative analysis of simultaneous, bilateral EEG recordings revealed a significant decrease of theta oscillations ipsilaterally during the latent phase and bilaterally during the chronic phase. Furthermore, the synchronization of bilateral activity, which is very high in control, was strongly reduced already during the latent phase and the decrease was independent of recurrent seizures. Immunohistochemical analysis performed in the contralateral hippocampus of kainate-treated mice revealed reduced calbindin-labeling of CA1 pyramidal cells; down-regulation of CCK-8 and up-regulation of NPY-labeling in mossy fibers; and a redistribution of galanin immunoreactivity. These changes collectively might limit neuronal excitability in CA1 and dentate gyrus, as well as glutamate release from mossy fiber terminals. Although these functional and neurochemical alterations might not be causally related, they likely reflect long-ranging network alterations underlying the independent evolution of the two hippocampal formations during the development of an epileptic focus in this model of TLE.

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Epileptogenesis and chronic seizures in a mouse model of temporal lobe epilepsy are associated with distinct EEG patterns and selective neurochemical alterations in the contralateral hippocampus

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