Enhanced nonsynaptic epileptiform activity in the dentate gyrus after kainate-induced status epilepticus

Highlights • NEA enhancement in the dentate gyrus is associated with increased neuronal NKCC1. • NEA suppression in CA1 is related to severe neuronal loss and glial proliferation. • NKCC1 blockage confirmed that the NKCC1 increase contributed to NEA changes in DG.

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Bibliographic Details
Published in:Neuroscience 2015-09, Vol.303, p.59-72
Main Authors: Nogueira, G.S, Santos, L.E.C, Rodrigues, A.M, Scorza, C.A, Scorza, F.A, Cavalheiro, E.A, de Almeida, A.-C.G
Format: Article
Language:English
Subjects:
Animals
Astrocytes - drug effects
Astrocytes - physiology
CA1 Region, Hippocampal - drug effects
CA1 Region, Hippocampal - metabolism
CA1 Region, Hippocampal - physiopathology
cation-chloride cotransporters
Cell Count
dentate gyrus
Dentate Gyrus - drug effects
Dentate Gyrus - metabolism
Dentate Gyrus - physiopathology
Disease Models, Animal
epilepsy
Excitatory Amino Acid Agonists - pharmacology
K Cl- Cotransporters
kainate model
Kainic Acid - pharmacology
Male
Microglia - drug effects
Microglia - physiology
Neurology
non-synaptic epileptiform activity
Pyramidal Cells - drug effects
Pyramidal Cells - metabolism
Pyramidal Cells - physiology
Rats, Wistar
Solute Carrier Family 12, Member 2 - metabolism
Status Epilepticus - chemically induced
Status Epilepticus - physiopathology
Symporters - metabolism
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Description
Summary:Highlights • NEA enhancement in the dentate gyrus is associated with increased neuronal NKCC1. • NEA suppression in CA1 is related to severe neuronal loss and glial proliferation. • NKCC1 blockage confirmed that the NKCC1 increase contributed to NEA changes in DG.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2015.06.057