Neuroscience 2002 Abstract
| Presentation Number: | 149.20 |
|---|---|
| Abstract Title: | Rap1B-activated MAP kinase regulates neuronal excitability and the threshold for certain forms of LTP. |
| Authors: |
Muzzio, I. A.*1
; Morozov, A.1
; Adams, P.3
; Sweatt, D.3
; Winder, D.4
; Cepeda, I.1
; Kandel, E. R.1,2
; Nolan, M. F.1
1Neurobiology & Behavior, Columbia University, New York, NY 2HHMI, New York, NY 3Baylor College of Medicine, Houston, TX 4Vanderbilt University, Nashville, TN |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Synaptic Plasticity -- Long-term potentiation (LTP) |
| Secondary Theme and Topics | Synaptic Transmission and Excitability<br />- Intrinsic Membrane Properties<br />-- Modulation of intrinsic membrane properties |
| Session: |
149. Synaptic plasticity: long-term potentiation I Poster |
| Presentation Time: | Sunday, November 3, 2002 4:00 PM-5:00 PM |
| Location: | Hall A2-B3 E-21 |
| Keywords: | excitability, Kv4.2, complex spikes, ERK |
Map kinase (MAPK) signaling is important for the induction and expression of certain forms of long-term potentiation (LTP). Using mice expressing a dominant negative Rap1B transgene, we found that in the hippocampus MAPK is modulated by Rap1B (Morozov et al., 1999, SFN abstracts, V22, 255.1). We have now used these mice to examine the contribution of Rap1B to the induction of LTP. Mutant mice have deficient LTP induction after either forskolin or theta frequency stimulation in area CA1 of the hippocampus. Inhibition of MAPK with UO126 (0.02 mM) causes a similar LTP induction deficit in wild-type mice, but does not further reduce LTP in mutant mice. Complex spike firing during theta frequency tetanization is reduced in mutant mice and during perfusion of UO126, suggesting that inhibition of the RAP1B/MAPK pathway decreases neuronal excitability. A corresponding decrease in excitability is also observed with whole-cell recordings from CA1 pyramidal neurons. The early LTP deficits and reduction in complex spikes is prevented when 4-AP (0.1 - 4 mM) is bath applied during induction, suggesting the involvement of A/D type potassium channels. In wild type but not mutant mice Kv4.2, the primary A type potassium channel in pyramidal cells, is phosphorylated following tetanic stimulation, indicating that potassium channels are modulated in response to synaptic activity. These data indicate that activation of MAPK via Rap1B mediates a dynamic, activity-dependent control of excitability in CA1 pyramidal cells.
Supported by HHMI & Mathers Foundation
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
Copyright © 2002-2026 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.
