Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Hippocampal long‐term potentiation is enhanced in urethane‐anesthetized RGS2 knockout mice

Hippocampal long‐term potentiation is enhanced in urethane‐anesthetized RGS2 knockout mice RGS2 is a member of the regulator of G‐protein signaling (RGS) family and has been implicated in cellular mechanisms associated with neuronal plasticity. Long‐term potentiation (LTP) of RGS2 knockout and wild‐type mice was examined at the Schaffer collaterals to CA1 pathway in urethane‐anesthetized mice in vivo to examine RGS2's possible role in the regulation of potentiation. As compared to wild‐type mice, RGS2 knockouts demonstrated much stronger LTP of the extracellular population spikes at the somatic and dendritic layers in CA1 region and more pronounced LTP of the population excitatory postsynaptic current sink. Under baseline conditions, RGS2 knockouts showed lower paired‐pulse facilitation of the excitatory postsynaptic potentials and associated current sinks in vivo as compared with wild‐type mice. The data show for the first time that RGS2 deficient mice in vivo differ from wild‐type mice in both short‐term and long‐term synaptic plasticity suggesting that RGS2 serves as a negative regulator of long‐term synaptic plasticity. © 2009 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hippocampus Wiley

Hippocampal long‐term potentiation is enhanced in urethane‐anesthetized RGS2 knockout mice

Loading next page...
 
/lp/wiley/hippocampal-long-term-potentiation-is-enhanced-in-urethane-HbO0PUGpzi

References (19)

Publisher
Wiley
Copyright
Copyright © 2009 Wiley‐Liss, Inc.
ISSN
1050-9631
eISSN
1098-1063
DOI
10.1002/hipo.20582
pmid
19294649
Publisher site
See Article on Publisher Site

Abstract

RGS2 is a member of the regulator of G‐protein signaling (RGS) family and has been implicated in cellular mechanisms associated with neuronal plasticity. Long‐term potentiation (LTP) of RGS2 knockout and wild‐type mice was examined at the Schaffer collaterals to CA1 pathway in urethane‐anesthetized mice in vivo to examine RGS2's possible role in the regulation of potentiation. As compared to wild‐type mice, RGS2 knockouts demonstrated much stronger LTP of the extracellular population spikes at the somatic and dendritic layers in CA1 region and more pronounced LTP of the population excitatory postsynaptic current sink. Under baseline conditions, RGS2 knockouts showed lower paired‐pulse facilitation of the excitatory postsynaptic potentials and associated current sinks in vivo as compared with wild‐type mice. The data show for the first time that RGS2 deficient mice in vivo differ from wild‐type mice in both short‐term and long‐term synaptic plasticity suggesting that RGS2 serves as a negative regulator of long‐term synaptic plasticity. © 2009 Wiley‐Liss, Inc.

Journal

HippocampusWiley

Published: Aug 1, 2009

There are no references for this article.