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J Physiol Volume 586, Number 9, 2263-2275, May 1, 2008 DOI: 10.1113/jphysiol.2007.142547
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NEUROSCIENCE

Involvement of AMPA receptor desensitization in short-term synaptic depression at the calyx of Held in developing rats

 Maki Koike-Tani1, Takeshi Kanda1, Naoto Saitoh1,2, Takayuki Yamashita1,3 and Tomoyuki Takahashi1,2,3

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

Paired-pulse facilitation (PPF) and depression (PPD) are forms of short-term plasticity that are generally thought to reflect changes in transmitter release probability. However, desensitization of postsynaptic AMPA receptors (AMPARs) significantly contributes to PPD at many glutamatergic synapses. To clarify the involvement of AMPAR desensitization in synaptic PPD, we compared PPD with AMPAR desensitization, induced by paired-pulse glutamate application in patches excised from postsynaptic cells at the calyx of Held synapse of developing rats. We found that AMPAR desensitization contributed significantly to PPD before the onset of hearing (P10–12), but that its contribution became negligible after hearing onset. During postnatal development (P7–21) the recovery of AMPARs from desensitization became faster. Concomitantly, glutamate sensitivity of AMPAR desensitization declined. Single-cell reverse transcription-polymerase chain reaction (RT-PCR) analysis indicated a developmental decline of GluR1 expression that correlated with speeding of the recovery of AMPARs from desensitization. Transmitter release probability declined during the second postnatal week (P7–14). Manipulation of the extracellular Ca2+/Mg2+ ratio, to match release probability at P7–8 and P13–15 synapses, revealed that the release probability is also an important factor determining the involvement of AMPAR desensitization in PPD. We conclude that the extent of involvement of AMPAR desensitization in short-term synaptic depression is determined by both pre- and postsynaptic mechanisms.

(Received 6 August 2007; accepted after revision 12 March 2008; first published online 13 March 2008)
Corresponding author T. Takahashi: Doshisha University Faculty of Life and Medical Sciences, 619-0225, Japan. Email: ttakahas{at}mail.doshisha.ac.jp

M. Koike-Tani and T. Kanda contributed equally to this study. This paper has online supplemental material.






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