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The Journal of Neuroscience, July 2, 2008, 28(27):6760-6772; doi:10.1523/JNEUROSCI.0643-08.2008

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Neurobiology of Disease
Synaptic Strength Modulation after Cortical Trauma: A Role in Epileptogenesis

Sinziana Avramescu and Igor Timofeev

Centre de Recherche Université Laval Robert-Giffard, Québec, Canada G1J 2G3

Correspondence should be addressed to Igor Timofeev, Centre de Recherche Université Laval Robert-Giffard, 2601, chemin de la Canardière, Québec, Canada G1J 2G3. Email: igor.timofeev{at}phs.ulaval.ca

Traumatic brain injuries are often followed by abnormal hyperexcitability, leading to acute seizures and epilepsy. Previous studies documented the rewiring capacity of neocortical neurons in response to various cortical and subcortical lesions. However, little information is available on the functional consequences of these anatomical changes after cortical trauma and the adaptation of synaptic connectivity to a decreased input produced by chronic deafferentation. In this study, we recorded intracellular (IC) activities of cortical neurons simultaneously with extracellular (EC) unit activities and field potentials of neighboring cells in cat cortex, after a large transection of the white matter underneath the suprasylvian gyrus, in acute and chronic conditions (at 2, 4, and 6 weeks) in ketamine–xylazine-anesthetized cats. Using EC spikes to compute the spike-triggered averages of IC membrane potential, we found an increased connection probability and efficacy between cortical neurons weeks after cortical trauma. Inhibitory interactions showed no significant changes in the traumatized cortex compared with control. The increased synaptic efficacy was accompanied by enhanced input resistance and intrinsic excitability of cortical neurons, as well as by increased duration of silent network periods. Our electrophysiological data revealed functional consequences of previously reported anatomical changes in the injured cortex. We suggest that homeostatic synaptic plasticity compensating the decreased activity in the undercut cortex leads to an uncontrollable cortical hyperexcitability and seizure generation.

Key words: epilepsy; cortical trauma; synaptic efficacy; intrinsic excitability; homeostatic plasticity; in vivo

Received Sept. 24, 2007; revised April 9, 2008; accepted April 14, 2008.

Correspondence should be addressed to Igor Timofeev, Centre de Recherche Université Laval Robert-Giffard, 2601, chemin de la Canardière, Québec, Canada G1J 2G3. Email: igor.timofeev{at}phs.ulaval.ca






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