title: Neocortical and thalamic spread of amygdala kindled seizures.
abstract: OBJECTIVE
  Amygdala kindling is an epilepsy model involving long-term network plasticity in the nervous system. In this model, repeated weak stimulation of the amygdala eventually leads to severe motor seizures. The mechanisms for worsening behavioral seizures, and the possible role of enhanced connectivity between the amygdala and other structures have not been thoroughly investigated.
  
  
  METHODS
  We performed simultaneous field potential recordings from the amygdala, frontal cortex, and medial thalamus during kindling in rats. Seizures were analyzed for signal power compared with baseline and for correlation between recording sites. Interictal signals were analyzed for changes in coherence between electrode contacts in kindled animals compared with sham kindled controls.
  
  
  RESULTS
  We found that increased behavioral severity of seizures was related to increased seizure duration and to increased signal power in the frontal cortex and medial thalamus. Kindling was associated with increased connectivity between the amygdala and frontal cortex, based on increased amygdala-frontal signal correlation during seizures. In addition, during the interictal period, increased coherence was noted between amygdala and frontal contacts in kindled animals compared with controls.
  
  
  CONCLUSIONS
  We found evidence for increased connectivity between the amygdala and frontal cortex both during seizures and in the interictal period, as a result of kindling. Enhanced connections between limbic and neocortical circuits may be important for the development of epilepsy, as well as for normal long-range network plasticity in the nervous system.
authors.affiliation: Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06520-8018, USA. hal.blumenfeld@yale.edu
authors.forename: Hal
authors.initials: H
authors.lastname: Blumenfeld
authors.forename: Maritza
authors.initials: M
authors.lastname: Rivera
authors.forename: J Gabriel
authors.initials: JG
authors.lastname: Vasquez
authors.forename: Akash
authors.initials: A
authors.lastname: Shah
authors.forename: Dina
authors.initials: D
authors.lastname: Ismail
authors.forename: Miro
authors.initials: M
authors.lastname: Enev
authors.forename: Hitten P
authors.initials: HP
authors.lastname: Zaveri
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005625:Frontal Lobe / Q000502:physiology; D007696:Kindling, Neurologic / Q000502:physiology*; D008297:Male; D019579:Neocortex / Q000502:physiology*; D009434:Neural Pathways / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000209:etiology / Q000503:physiopathology*; D013788:Thalamus / Q000502:physiology