Mg2+ Block of Drosophila

By T. Miyashita, Y. Oda, J. Horiuchi, J. Yin, T. Morimoto, M. Saitoe. 2012

104 citations recorded by the source corpus.

SUMMARY NMDA receptor (NMDAR) channels allow Ca2+ influx only during correlated activation of both pre- and postsynaptic cells; a Mg2+ block mechanism suppresses NMDAR activity when the postsynaptic cell is inactive. Although the importance of NMDARs in associative learning and long-term memory (LTM) formation has been demonstrated, the role of Mg2+ block in these processes remains unclear. Using transgenic flies expressing NMDARs defective for Mg2+ block, we found that Mg2+ block mutants are defective for LTM formation but not associative learning. We demonstrate that LTM-dependent increases in expression of synaptic genes, including homer, staufen, and activin, are abolished in flies expressing Mg2+ block defective NMDARs. Furthermore, we show that genetic and pharmacological reduction of Mg2+ block significantly increases expression of a CREB repressor isoform. Our results suggest that Mg2+ block of NMDARs functions to suppress basal expression of a CREB repressor, thus permitting CREB-dependent gene expression upon LTM induction.

Subfields: Cell Biology, Cellular and Molecular Neuroscience

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In Cellular and Molecular Neuroscience

  1. Yoshinori Aso
  2. Gerald M. Rubin
  3. Hiromu Tanimoto
  4. S. Waddell
  5. P. Plaçais
  6. T. Préat
  7. Nobuhiro Yamagata
  8. Toshiharu Ichinose

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