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This Article Full Text Full Text (PDF) All Versions of this Article: 586/9/2253    most recent jphysiol.2007.142521v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Nakamura, T. Articles by Takahashi, T. PubMed PubMed Citation Articles by Nakamura, T. Articles by Takahashi, T. Related Collections Neuroscience

¹ Department of Neurophysiology, University of Tokyo Graduate School of Medicine, Tokyo 113-0033, Japan
² Department of Neurophysiology, Doshisha University Faculty of Life and Medical Sciences, Kyoto 619-0225, Japan
³ Cellular & Molecular Synaptic Function Unit, Initial Research Project (IRP), Okinawa Institute of Science and Technology Promotion Corporation (OIST), Okinawa 904-2234, Japan

Ca²⁺-binding to calmodulin (CaM) causes facilitation and/or inactivation of recombinant Ca²⁺ channels. At the rat calyx of Held, before hearing onset, presynaptic Ca²⁺ currents (I_pCa) undergo Ca²⁺/CaM-dependent inactivation during repetitive activation at around 1 Hz, implying that this may be a major cause of short-term synaptic depression. However, it remains open whether the Ca²⁺/CaM-dependent inactivation of I_pCa persists in more mature animals. To address this question, we tested the effect of CaM inhibitors on the activity-dependent modulation of I_pCa in calyces, before (postnatal day (P) 7–9) and after (P13–15) hearing onset. Our results indicate that the CaM-dependent I_pCa inactivation during low-frequency stimulation, and the ensuing synaptic depression, occur only at calyces in the prehearing period. However, CaM immunoreactivity in P8 and P14 calyces was equally strong. Even at P13–15, high frequency stimulation (200–500 Hz) could induce I_pCa inactivation, which was attenuated by EGTA (10 mM) or a CaM inhibitor peptide loaded into the terminal. Furthermore, the CaM inhibitor peptide attenuated a transient facilitation of I_pCa preceding inactivation observed at 500 Hz stimulation, whereas it had no effect on sustained I_pCa facilitations during trains of 50–200 Hz stimulation. These results suggest that the Ca²⁺/CaM-dependent I_pCa modulation requires a high intraterminal Ca²⁺ concentration, which can be attained at immature calyces during low frequency stimulation, but only during unusually high frequency stimulation at calyceal terminals in the posthearing period.

(Received 6 August 2007; accepted after revision 25 January 2008; first published online 31 January 2008)
Corresponding author T. Takahashi: Doshisha University, Faculty of Life and Medical Sciences, Kyoto 619-0225, Japan. Email: ttakahas{at}mail.doshisha.ac.jp

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