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Structural plasticity of dentate granule cell mossy fibers during the development of limbic epilepsy
Author(s) -
Danzer Steve C.,
He Xiaoping,
Loepke Andreas W.,
McNamara James O.
Publication year - 2010
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20589
Subject(s) - epileptogenesis , neuroscience , granule cell , inhibitory postsynaptic potential , epilepsy , synaptic plasticity , mossy fiber (hippocampus) , gabaergic , pyramidal cell , pilocarpine , excitatory postsynaptic potential , chemistry , biology , hippocampal formation , dentate gyrus , receptor , biochemistry
Altered granule cell≫CA3 pyramidal cell synaptic connectivity may contribute to the development of limbic epilepsy. To explore this possibility, granule cell giant mossy fiber bouton plasticity was examined in the kindling and pilocarpine models of epilepsy using green fluorescent protein‐expressing transgenic mice. These studies revealed significant increases in the frequency of giant boutons with satellite boutons 2 days and 1 month after pilocarpine status epilepticus, and increases in giant bouton area at 1 month. Similar increases in giant bouton area were observed shortly after kindling. Finally, both models exhibited plasticity of mossy fiber giant bouton filopodia, which contact GABAergic interneurons mediating feedforward inhibition of CA3 pyramids. In the kindling model, however, all changes were fleeting, having resolved by 1 month after the last evoked seizure. Together, these findings demonstrate striking structural plasticity of granule cell mossy fiber synaptic terminal structure in two distinct models of adult limbic epileptogenesis. We suggest that these plasticities modify local connectivities between individual mossy fiber terminals and their targets, inhibitory interneurons, and CA3 pyramidal cells potentially altering the balance of excitation and inhibition during the development of epilepsy. © 2009 Wiley‐Liss, Inc.