PURPOSE: In limbic or mesial temporal lobe epilepsy, much attention has been given to specific regions or cell populations (e.g., the hippocampus or dentate granule cells). Epileptic seizures may involve broader changes in neural circuits, and evidence suggests that subcortical regions may play a role. In this study we examined the midline thalamic regions for involvement in limbic seizures, changes in anatomy and physiology, and the potential role for this region in limbic seizures and epilepsy. METHODS: Using two rat models for limbic epilepsy (hippocampal kindled and chronic spontaneous limbic epilepsy) we examined the midline thalamus for evidence of involvement in seizure activity, alterations in structure, changes in the basic in vitro physiology of the thalamic neurons. We also explored how this region may influence limbic seizures. RESULTS: The midline thalamus was consistently involved with seizure activity from the onset, and there was significant neuronal loss in the medial dorsal and reuniens/rhomboid nuclei. In addition, thalamic neurons had changes in synaptically mediated and voltage-gated responses. Infusion of lidocaine into the midline thalamus significantly shortened afterdischarge duration. CONCLUSIONS: These observations suggest that this thalamic region is part of the neural circuitry of limbic epilepsy and may play a significant role in seizure modulation. Local neuronal changes can enhance the excitability of the thalamolimbic circuits.
PURPOSE: In limbic or mesial temporal lobe epilepsy, much attention has been given to specific regions or cell populations (e.g., the hippocampus or dentate granule cells). Epilepticseizures may involve broader changes in neural circuits, and evidence suggests that subcortical regions may play a role. In this study we examined the midline thalamic regions for involvement in limbic seizures, changes in anatomy and physiology, and the potential role for this region in limbic seizures and epilepsy. METHODS: Using two rat models for limbic epilepsy (hippocampal kindled and chronic spontaneous limbic epilepsy) we examined the midline thalamus for evidence of involvement in seizure activity, alterations in structure, changes in the basic in vitro physiology of the thalamic neurons. We also explored how this region may influence limbic seizures. RESULTS: The midline thalamus was consistently involved with seizure activity from the onset, and there was significant neuronal loss in the medial dorsal and reuniens/rhomboid nuclei. In addition, thalamic neurons had changes in synaptically mediated and voltage-gated responses. Infusion of lidocaine into the midline thalamus significantly shortened afterdischarge duration. CONCLUSIONS: These observations suggest that this thalamic region is part of the neural circuitry of limbic epilepsy and may play a significant role in seizure modulation. Local neuronal changes can enhance the excitability of the thalamolimbic circuits.
Authors: Jean-Christophe Cassel; Anne Pereira de Vasconcelos; Michaël Loureiro; Thibault Cholvin; John C Dalrymple-Alford; Robert P Vertes Journal: Prog Neurobiol Date: 2013-09-08 Impact factor: 11.685
Authors: Christopher C Stewart; H Randall Griffith; Ozioma C Okonkwo; Roy C Martin; Robert K Knowlton; Elizabeth J Richardson; Bruce P Hermann; Michael Seidenberg Journal: Brain Cogn Date: 2008-07-02 Impact factor: 2.310
Authors: Dalin T Pulsipher; Michael Seidenberg; Jared J Morton; Elizabeth Geary; Joy Parrish; Bruce Hermann Journal: Epilepsy Behav Date: 2007-11 Impact factor: 2.937
Authors: Dalin T Pulsipher; Michael Seidenberg; Leslie Guidotti; Victoria N Tuchscherer; Jared Morton; Raj D Sheth; Bruce Hermann Journal: Epilepsia Date: 2009-01-17 Impact factor: 5.864