title: The midline thalamus: alterations and a potential role in limbic epilepsy.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Neurology, University of Virginia, Charlottesville, Virginia 22908, USA. ehb2z@virginia.edu
authors.forename: E H
authors.initials: EH
authors.lastname: Bertram
authors.forename: P S
authors.initials: PS
authors.lastname: Mangan
authors.forename: D
authors.initials: D
authors.lastname: Zhang
authors.forename: C A
authors.initials: CA
authors.lastname: Scott
authors.forename: J M
authors.initials: JM
authors.lastname: Williamson
mesh_terms: D019412:Anatomy, Cross-Sectional; D000818:Animals; D002452:Cell Count; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D004833:Epilepsy, Temporal Lobe / Q000503:physiopathology*; D006624:Hippocampus / Q000166:cytology / Q000502:physiology / Q000503:physiopathology; D007696:Kindling, Neurologic / Q000502:physiology; D008012:Lidocaine / Q000494:pharmacology; D008032:Limbic System / Q000166:cytology / Q000502:physiology / Q000503:physiopathology*; D008297:Male; D009434:Neural Pathways / Q000166:cytology / Q000502:physiology / Q000503:physiopathology; D009474:Neurons / Q000166:cytology / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013787:Thalamic Nuclei / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D013788:Thalamus / Q000166:cytology / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D008012:Lidocaine