Components of NMDA-induced Ca<SUP>2+</SUP> signal in mouse hippocampal slices and acute effects of corticosterone on each component

DOI 1 Citations 21 References
  • Osanai Hiromi
    Department of Correlative Study in Physics and Chemistry, Graduate School of Integrated Basic Sciences, Nihon University
  • Suzuki Akiyoshi
    Department of Correlative Study in Physics and Chemistry, Graduate School of Integrated Basic Sciences, Nihon University
  • Komatsuzaki Yoshimasa
    Department of Correlative Study in Physics and Chemistry, Graduate School of Integrated Basic Sciences, Nihon University
  • Hirano-Iwata Ayumi
    Graduate School of Biomedical Engineering, Tohoku University
  • Kawato Suguru
    Department of Biophysics and Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo
  • Saito Minoru
    Department of Correlative Study in Physics and Chemistry, Graduate School of Integrated Basic Sciences, Nihon University

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N-methyl-D-aspartate (NMDA) stimulation is usually used to investigate a series of neuronal mechanisms involved in NMDA receptor-mediated Ca2+ signal. We here examined by using Ca2+ imaging technique whether the NMDA-induced Ca2+ signal is due to the exclusive activation of NMDA receptors or activation of voltage-dependent calcium channels (VDCCs) together with NMDA receptors in mouse hippocampal slices. In order to isolate each component of the Ca2+ signal, we used sodium channel antagonist tetrodotoxin (TTX), which prevents dendritic spikes and the following activation of VDCCs, and L-type VDCC antagonist nicardipine. The results showed that in the CA1 region, almost a half of the NMDA-induced Ca2+ signal was the TTX-sensitive component involved in indirect Ca2+ influx via VDCCs, while the other half was the TTX-insensitive component involved in direct Ca2+ influx via NMDA receptors. In addition, the TTX-sensitive component should be almost via L-type VDCCs. We further examined the effects of corticosterone (CORT), which is a principal glucocorticoid synthesized in the rodent adrenal cortex and secreted in response to stress, on each component. It has been reported that CORT acutely (nongenomically) suppress the NMDA-induced Ca2+ signal in the CA1 region. The present results, however, led us to a new finding that CORT enhanced the TTX-insensitive component and the suppressive effect of CORT reported so far should be attributed to the effect on the TTX-sensitive component.

Journal

  • bioimages

    bioimages 16 (0), 31-37, 2008

    Bioimaging Society

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