title: Imbalance of interneuron distribution between neocortex and basal ganglia: consideration of epileptogenesis of focal cortical dysplasia.
abstract: OBJECTIVE
  The balance of excitation and inhibition of neurons and neuronal network is very important to perform complete neuronal function. Damage or loss of inhibitory γ-aminobutyric acid (GABA)-ergic interneuron is associated with impaired inhibitory control of cortical pyramidal neurons, leading to hyperexcitability and epileptogenesis. Ectopic neurons in the basal ganglia are to be one of the pathological features of epileptogenesis. In the present study, we investigated distribution of interneuron subtypes between neocortex and caudate nucleus.
  
  
  METHODS
  We performed immunohistochemistry of GABA, glutamic acid decarboxylase (GAD), calretinin (CR), calbindin (CB), parvalbumin (PV) and neuropeptide. We used surgical materials of four focal cortical dysplasia (FCD) cases, having lesions of neocortex and caudate nucleus, and eight age-matched autopsy controls.
  
  
  RESULTS
  The pathology showed three FCD IIa, containing dysmorphic neurons, and one FCD IIb, balloon cells. In the neocortex, the concentrations (each positive cell number/all cell numbers in the evaluated field) of GAD+, CR+ and CB+ cells were significantly lower in FCD than in controls. On the contrary, in the caudate nucleus those of CR+ and CB+ cells were significantly more in FCD than in controls.
  
  
  CONCLUSIONS
  The interneuron imbalance between the neocortex and basal ganglia may affect the epileptogenesis of FCD.
authors.affiliation: Epilepsy Center, National Center of Neurology and Psychiatry, Kodaira, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sakakibara
authors.forename: S
authors.initials: S
authors.lastname: Sukigara
authors.forename: T
authors.initials: T
authors.lastname: Otsuki
authors.forename: A
authors.initials: A
authors.lastname: Takahashi
authors.forename: Y
authors.initials: Y
authors.lastname: Kaneko
authors.forename: T
authors.initials: T
authors.lastname: Kaido
authors.forename: Y
authors.initials: Y
authors.lastname: Saito
authors.forename: N
authors.initials: N
authors.lastname: Sato
authors.forename: E
authors.initials: E
authors.lastname: Nakagawa
authors.forename: K
authors.initials: K
authors.lastname: Sugai
authors.forename: M
authors.initials: M
authors.lastname: Sasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: M
authors.initials: M
authors.lastname: Itoh
mesh_terms: D000293:Adolescent; D001927:Brain Diseases / Q000150:complications / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D064032:Calbindin 2; D064026:Calbindins; D016022:Case-Control Studies; D002421:Caudate Nucleus / Q000473:pathology* / Q000601:surgery; D002452:Cell Count; D002648:Child; D002675:Child, Preschool; D004828:Epilepsies, Partial / Q000209:etiology* / Q000503:physiopathology / Q000601:surgery; D004827:Epilepsy; D005260:Female; D059330:GABAergic Neurons / Q000737:chemistry / Q000473:pathology*; D005968:Glutamate Decarboxylase / Q000032:analysis; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007395:Interneurons / Q000737:chemistry / Q000145:classification / Q000473:pathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D054220:Malformations of Cortical Development / Q000150:complications / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D065703:Malformations of Cortical Development, Group I; D019579:Neocortex / Q000473:pathology* / Q000601:surgery; D009419:Nerve Tissue Proteins / Q000032:analysis; D009479:Neuropeptides / Q000032:analysis; D010320:Parvalbumins / Q000032:analysis; D064030:S100 Calcium Binding Protein G / Q000032:analysis; D005680:gamma-Aminobutyric Acid / Q000032:analysis
chemical_list: C576764:CALB2 protein, human; D064032:Calbindin 2; D064026:Calbindins; D009419:Nerve Tissue Proteins; D009479:Neuropeptides; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase