Neuroscience 2003 Abstract
| Presentation Number: | 55.7 |
|---|---|
| Abstract Title: | The immediate-early gene arc regulates AMPA-receptor trafficking. |
| Authors: |
Rial Verde, E. M.*1
; Worley, P.2
; Malinow, R.1
; Cline, H. T.1
1Cold Spring Harbor Lab, Cold Spring Harbor, NY 2MD, 1 Bungtown Rd, 11724, |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Synaptic Transmission -- Postsynaptic mechanisms: Excitatory |
| Session: |
55. Postsynaptic Mechanisms: Excitatory II Poster |
| Presentation Time: | Saturday, November 8, 2003 3:00 PM-4:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # F22 |
| Keywords: | GluR2, LTD, synaptic depression, rat hippocampus |
The immediate-early gene ARC is induced by neuronal activity (Lyford et al., 1995, Neuron 14:433). In addition, its mRNA is selectively transported to the activated portion of the dendritic arbor after high frequency synaptic stimulation (Steward et al., 1998, Neuron 21:741). We have previously shown that after the ARC protein reaches synaptic sites, it induces an AMPA-receptor specific synaptic depression. Moreover, drugs that affect protein phosphatase activity reduce the ARC-induced depression (Rial Verde et al., 2002, SFN 32nd Annual Meeting Abstract 839.5). The latter result suggests that ARC-induced depression may share some molecular mechanisms with other forms of synaptic depression. Here we investigate the AMPA-receptor subunit specificity of the ARC effect and further explore the molecular events that result in ARC-induced synaptic depression.
Fluorescently-tagged proteins were expressed in CA1 pyramidal neurons of cultured hippocampal slices using a Sindbis virus expression system. The slices were cut from P7 rats and cultured for 6-9 days before infection. 10-18hs after infection whole-cell patch clamp recordings were simultaneusly obtained from infected and nearby non-infected control cells.
The C-terminal cytoplasmic tail of the GluR2 subunit of the AMPA-receptor has been extensively involved in AMPA receptor trafficking. Ectopic expression of the GluR2 C-tail in hippocampal neurons causes run-down of basal synaptic transmission and interferes with LTD. We coexpressed GluR2 C-tail and ARC to test the involvement of the GluR2-dependent AMPA receptor trafficking in ARC-induced depression. GluR2 C-tail and ARC coexpression caused the same amount of depression as either ARC or GluR2 C-tail alone. These results suggest that ARC-induced depression operates by altering the GluR2-dependent AMPA-receptor trafficking pathway.
Fluorescently-tagged proteins were expressed in CA1 pyramidal neurons of cultured hippocampal slices using a Sindbis virus expression system. The slices were cut from P7 rats and cultured for 6-9 days before infection. 10-18hs after infection whole-cell patch clamp recordings were simultaneusly obtained from infected and nearby non-infected control cells.
The C-terminal cytoplasmic tail of the GluR2 subunit of the AMPA-receptor has been extensively involved in AMPA receptor trafficking. Ectopic expression of the GluR2 C-tail in hippocampal neurons causes run-down of basal synaptic transmission and interferes with LTD. We coexpressed GluR2 C-tail and ARC to test the involvement of the GluR2-dependent AMPA receptor trafficking in ARC-induced depression. GluR2 C-tail and ARC coexpression caused the same amount of depression as either ARC or GluR2 C-tail alone. These results suggest that ARC-induced depression operates by altering the GluR2-dependent AMPA-receptor trafficking pathway.
Supported by Supported by: HHMI and David and Fanny Luke (EMRV) and NIH
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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