Neuroscience 2002 Abstract
| Presentation Number: | 150.1 |
|---|---|
| Abstract Title: | SNARE-DEPENDENT REGULATION OF SYNAPTIC AMPA RECEPTORS DURING POSTSYNAPTIC IP<sub>3</sub> RECEPTOR MEDIATED INTRACELLULAR Ca<sup>2+</sup> RELEASE. |
| Authors: |
Maher, B.*2
; Mac Kinnon II, R. L.2
; Bai, J.1
; Chapman, E. R.1
; Kelly, P. T.2
1Dept. of Physiology, University of Wisconsin, Madison, WI 2Dept. of Molecular Biosciences, University of Kansas, Lawrence, KS |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Synaptic Plasticity -- Long-term potentiation (LTP) |
| Secondary Theme and Topics | Synaptic Transmission and Excitability<br />- Synaptic Transmission<br />-- Postsynaptic mechanisms: Excitatory |
| Session: |
150. Synaptic plasticity: long-term potentiation II Poster |
| Presentation Time: | Sunday, November 3, 2002 1:00 PM-2:00 PM |
| Location: | Hall A2-B3 E-41 |
| Keywords: | Glutamate Receptors, Excitatory Neurotransmission, Receptor Trafficking, Synaptic Plasticity |
Changes in the number of synaptic AMPARs appears to be an important mechanism that regulates synaptic plasticity. We have shown that postsynaptic perfusion (whole-cell) of the IP3R agonist adenophostin strongly potentiates AMPA receptor-mediated EPSCs. This potentiation is blocked by BAPTA and depends on PDZ-domain interactions, suggesting that intracellular Ca2+ release modulates the function and/or stability of synaptic AMPARs (Maher and Kelly, SFN Abstr. # 923.2, 2001).
Since intracellular Ca2+ release leads to an increase in synaptic AMPAR function, then SNARE-dependent exocytosis may be necessary to insert new AMPARs at synapses. To examine the latter postulate, we co-perfused adenophostin plus a recombinant synaptotagmin peptide consisting of tandem C2A domains (C2A-C2A) that inhibits exocytosis in permeabilized PC12 cells (Earles et al., 2001). Co-perfusion of C2A-C2A plus adenophostin strongly attenuated increases in EPSC amplitudes compared to adenophostin alone, suggesting that postsynaptic intracellular Ca2+ release alters AMPAR trafficking and stabilization through a SNARE-dependent mechanism. Postsynaptic perfusion of C2A-C2A alone also caused a significant run-down of EPSC amplitudes, suggesting that AMPARs constitutively cycle in a SNARE-regulated manner to maintain basal levels of synaptic transmission. These results suggest that postsynaptic AMPAR cycling/trafficking is regulated by SNARE-dependent mechanisms during basal and potentiated synaptic transmission.
Since intracellular Ca2+ release leads to an increase in synaptic AMPAR function, then SNARE-dependent exocytosis may be necessary to insert new AMPARs at synapses. To examine the latter postulate, we co-perfused adenophostin plus a recombinant synaptotagmin peptide consisting of tandem C2A domains (C2A-C2A) that inhibits exocytosis in permeabilized PC12 cells (Earles et al., 2001). Co-perfusion of C2A-C2A plus adenophostin strongly attenuated increases in EPSC amplitudes compared to adenophostin alone, suggesting that postsynaptic intracellular Ca2+ release alters AMPAR trafficking and stabilization through a SNARE-dependent mechanism. Postsynaptic perfusion of C2A-C2A alone also caused a significant run-down of EPSC amplitudes, suggesting that AMPARs constitutively cycle in a SNARE-regulated manner to maintain basal levels of synaptic transmission. These results suggest that postsynaptic AMPAR cycling/trafficking is regulated by SNARE-dependent mechanisms during basal and potentiated synaptic transmission.
Supported by PHS grant to Dr. Paul T. Kelly
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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