Neuroscience 2003 Abstract
| Presentation Number: | 56.2 |
|---|---|
| Abstract Title: | IP<sub>3</sub> receptor mediated intracellular Ca<sup>2+</sup> release can enhance NMDA EPCSs in CA1 neurons. |
| Authors: |
MacKinnon, R. L.*1
; Maher, B.1
; Kelly, P. T.1
1Mol. BioSci., Univ. of Kansas, Lawrence, KS |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Synaptic Plasticity -- Long-term potentiation (LTP) |
| Session: |
56. LTP/LTD Modulation Poster |
| Presentation Time: | Saturday, November 8, 2003 2:00 PM-3:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # F42 |
| Keywords: | NMDA RECEPTOR, HIPPOCAMPUS, SYNAPTIC TRANSMISSION, LTP |
There is good evidence that changing the number of synaptic AMPARs is an important mechanism underlying synaptic plasticity. We have shown that whole-cell perfusion of the IP3R agonist adenophostin strongly potentiates AMPA receptor-mediated EPSCs via intracellular Ca2+ release (Maher and Kelly, SFN Abstr. # 923.2, 2001), and this potentiation is mediated through a SNARE-dependent mechanism (Maher, et.al., SFN Abstr. # 150.1, 2002). Recently, the trafficking of synaptic NMDARs has been shown to be associated with synaptic plasticity (Carroll and Zukin, TINS 2002, 25(11):571-7). We are exploring the possibility that intracellular Ca2+ release can modulate postsynaptic NMDA EPSCs. We observed that whole-cell perfusion of adenophostin can significantly increase pharmacologically isolated NMDA EPSCs monitored in ACSF containing 0.8 mM Mg2+, 10 µM CNQX, and 50 µM PTX at -30 mV holding potential. In addition, co-perfusion of 5 mM BAPTA can block the intracellular Ca2+-induced increase in NMDA EPSCs observed with adenophostin alone. These results suggest that IP3R-mediated postsynaptic Ca2+ release can modulate both NMDA- and AMPA-type synaptic receptors.
Supported by PHS grant to Paul Kelly
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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