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The Journal of Neuroscience, April 29, 2009, 29(17):5402-5410; doi:10.1523/JNEUROSCI.4699-08.2009

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Neurobiology of Disease
Early Deficits in Spatial Memory and Theta Rhythm in Experimental Temporal Lobe Epilepsy

Laetitia Chauvière,¹ Nadia Rafrafi,¹ Catherine Thinus-Blanc,¹ Fabrice Bartolomei,^1,2 Monique Esclapez,¹ and Christophe Bernard¹

¹Inserm–U751, Université de la Méditerranée, 13005 Marseille, France, and ²Assistance Publique des Hôpitaux de Marseille Hôpital La Timone, 13005 Marseille, France

Correspondence should be addressed to Laetitia Chauvière, Inserm–U751, Université de la Méditerranée, 27, Boulevard Jean Moulin, 13005 Marseille, France. Email: laetitia.chauviere{at}univmed.fr

Patients with temporal lobe epilepsy (TLE), the most common form of epilepsy in adults, often display cognitive deficits. The time course and underlying mechanisms of cognitive decline remain unknown during epileptogenesis (the process leading to epilepsy). Using the rat pilocarpine model of TLE, we performed a longitudinal study to assess spatial and nonspatial cognitive performance during epileptogenesis. In parallel, we monitored interictal-like activity (ILA) in the hippocampal CA1 region, as well as theta oscillations, a brain rhythm central to numerous cognitive processes. Here, we report that spatial memory was altered soon after pilocarpine-induced status epilepticus, i.e., already during the seizure-free, latent period. Spatial deficits correlated with a decrease in the power of theta oscillations but not with the frequency of ILA. Spatial deficits persisted when animals had spontaneous seizures (chronic stage) without further modification. In contrast, nonspatial memory performances remained unaffected throughout. We conclude that the reorganization of hippocampal circuitry that immediately follows the initial insult can affect theta oscillation mechanisms, in turn, resulting in deficits in hippocampus-dependent memory tasks. These deficits may be dissociated from the process that leads to epilepsy itself but could instead constitute, as ILA, early markers in at-risk patients and/or provide beneficial therapeutic targets.

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Received Sept. 30, 2008; revised Feb. 23, 2009; accepted Feb. 27, 2009.

Correspondence should be addressed to Laetitia Chauvière, Inserm–U751, Université de la Méditerranée, 27, Boulevard Jean Moulin, 13005 Marseille, France. Email: laetitia.chauviere{at}univmed.fr

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