Pannexin 1 regulates bidirectional hippocampal synaptic plasticity in adult mice
The threshold for bidirectional modification of synaptic plasticity is known to be controlled by several factors, including the balance between protein phosphorylation and dephosphorylation, postsynaptic free Ca(2+) concentration and NMDA receptor (NMDAR) composition of GluN2 subunits. Pannexin 1 (P...
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Published in | Frontiers in cellular neuroscience Vol. 8; p. 326 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Research Foundation
15.10.2014
Frontiers Media S.A |
Subjects | |
Online Access | Get full text |
ISSN | 1662-5102 1662-5102 |
DOI | 10.3389/fncel.2014.00326 |
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Summary: | The threshold for bidirectional modification of synaptic plasticity is known to be controlled by several factors, including the balance between protein phosphorylation and dephosphorylation, postsynaptic free Ca(2+) concentration and NMDA receptor (NMDAR) composition of GluN2 subunits. Pannexin 1 (Panx1), a member of the integral membrane protein family, has been shown to form non-selective channels and to regulate the induction of synaptic plasticity as well as hippocampal-dependent learning. Although Panx1 channels have been suggested to play a role in excitatory long-term potentiation (LTP), it remains unknown whether these channels also modulate long-term depression (LTD) or the balance between both types of synaptic plasticity. To study how Panx1 contributes to excitatory synaptic efficacy, we examined the age-dependent effects of eliminating or blocking Panx1 channels on excitatory synaptic plasticity within the CA1 region of the mouse hippocampus. By using different protocols to induce bidirectional synaptic plasticity, Panx1 channel blockade or lack of Panx1 were found to enhance LTP, whereas both conditions precluded the induction of LTD in adults, but not in young animals. These findings suggest that Panx1 channels restrain the sliding threshold for the induction of synaptic plasticity and underlying brain mechanisms of learning and memory. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Reviewed by: Nora Prochnow, Ruhr-Universität Bochum, Germany; Leigh Anne Swayne, University of Victoria, Canada; Andrei Belousov, University of Kansas Medical Center, USA This article was submitted to the journal Frontiers in Cellular Neuroscience. Edited by: Jonathan Mapelli, University of Modena and Reggio Emilia, Italy |
ISSN: | 1662-5102 1662-5102 |
DOI: | 10.3389/fncel.2014.00326 |