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Intracellular Zn 2+ signaling in the dentate gyrus is required for object recognition memory
Author(s) -
Takeda Atsushi,
Tamano Haruna,
Ogawa Taisuke,
Takada Shunsuke,
Nakamura Masatoshi,
Fujii Hiroaki,
Ando Masaki
Publication year - 2014
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.22322
Subject(s) - dentate gyrus , long term potentiation , granule cell , chemistry , neuroscience , intracellular , extracellular , perforant pathway , granule (geology) , microbiology and biotechnology , perforant path , hippocampus , biochemistry , biology , receptor , paleontology
The role of perforant pathway‐dentate granule cell synapses in cognitive behavior was examined focusing on synaptic Zn 2+ signaling in the dentate gyrus. Object recognition memory was transiently impaired when extracellular Zn 2+ levels were decreased by injection of clioquinol and N , N , N ′, N ′ ‐t etrakis‐(2‐pyridylmethyl) ethylendediamine. To pursue the effect of the loss and/or blockade of Zn 2+ signaling in dentate granule cells, ZnAF‐2DA (100 pmol, 0.1 mM/1 µl), an intracellular Zn 2+ chelator, was locally injected into the dentate molecular layer of rats. ZnAF‐2DA injection, which was estimated to chelate intracellular Zn 2+ signaling only in the dentate gyrus, affected object recognition memory 1 h after training without affecting intracellular Ca 2+ signaling in the dentate molecular layer. In vivo dentate gyrus long‐term potentiation (LTP) was affected under the local perfusion of the recording region (the dentate granule cell layer) with 0.1 mM ZnAF‐2DA, but not with 1 – 10 mM CaEDTA, an extracellular Zn 2+ chelator, suggesting that the blockade of intracellular Zn 2+ signaling in dentate granule cells affects dentate gyrus LTP. The present study demonstrates that intracellular Zn 2+ signaling in the dentate gyrus is required for object recognition memory, probably via dentate gyrus LTP expression. © 2014 Wiley Periodicals, Inc.

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