scholarly journals Impaired Conditioned Fear and Enhanced Long-Term Potentiation inFmr2 Knock-Out Mice

2002 ◽  
Vol 22 (7) ◽  
pp. 2753-2763 ◽  
Author(s):  
Yanghong Gu ◽  
Kellie L. McIlwain ◽  
Edwin J. Weeber ◽  
Takanori Yamagata ◽  
Bisong Xu ◽  
...  
Keyword(s):  
Conditioned Fear ◽  
Long Term Potentiation ◽  
Knock Out ◽  
Term Potentiation ◽  
Knock Out Mice

scholarly journals Long-term depression is independent of GluN2 subunit composition

2018 ◽  
Author(s):  
Jonathan M. Wong ◽  
John A. Gray
Keyword(s):  
Long Term Potentiation ◽  
Subunit Composition ◽  
Long Term Depression ◽  
Major Question ◽  
Knock Out ◽  
Single Receptor ◽  
Term Potentiation ◽  
Nmdar Subunit ◽  
Knock Out Mice

AbstractNMDA receptors (NMDARs) mediate major forms of both long-term potentiation (LTP) and long-term depression (LTD) and understanding how a single receptor can initiate both phenomena remains a major question in neuroscience. A prominent hypothesis implicates the NMDAR subunit composition, specifically GluN2A and GluN2B, in dictating the rules of synaptic plasticity. However, studies testing this hypotheses have yielded inconsistent and often contradictory results, especially for LTD. These inconsistent results may be due to challenges in the interpretation of subunit-selective pharmacology and in dissecting out the contributions of differential channel properties versus the interacting proteins unique to GluN2A or GluN2B. In this study, we address the pharmacological and biochemical challenges by utilizing a single-neuron genetic approach to delete NMDAR subunits in both male and female conditional knock-out mice. In addition, emerging evidence that non-ionotropic signaling through the NMDAR is sufficient for NMDAR-dependent LTD allowed the rigorous assessment of unique subunit contributions to NMDAR-dependent LTD while eliminating the variable of differential charge transfer. Here we find that neither the GluN2A nor the GluN2B subunit is strictly necessary for either non-ionotropic or ionotropic LTD.

scholarly journals Enhanced Hippocampal Long-Term Potentiation and Spatial Learning in Aged 11 -Hydroxysteroid Dehydrogenase Type 1 Knock-Out Mice

2007 ◽  
Vol 27 (39) ◽  
pp. 10487-10496 ◽  
Author(s):  
J. L. W. Yau ◽  
K. M. McNair ◽  
J. Noble ◽  
D. Brownstein ◽  
C. Hibberd ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Hydroxysteroid Dehydrogenase ◽  
Long Term Potentiation ◽  
Knock Out ◽  
Term Potentiation ◽  
Knock Out Mice

scholarly journals Inducible molecular switches for the study of long-term potentiation

2003 ◽  
Vol 358 (1432) ◽  
pp. 797-804 ◽  
Author(s):  
Gaël Hédou ◽  
Isabelle M. Mansuy
Keyword(s):  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Knock Out ◽  
Technical Developments ◽  
Term Potentiation ◽  
Dependent Protein ◽  
Strength And Plasticity ◽  
Regulated Gene Expression ◽  
Molecular Bases

This article reviews technical and conceptual advances in unravelling the molecular bases of long-term potentiation (LTP), learning and memory using genetic approaches. We focus on studies aimed at testing a model suggesting that protein kinases and protein phosphatases balance each other to control synaptic strength and plasticity. We describe how gene ‘knock-out’ technology was initially exploited to disrupt the Ca 2+ /calmodulin-dependent protein kinase II α (CaMKII α ) gene and how refined knock-in techniques later allowed an analysis of the role of distinct phosphorylation sites in CaMKII. Further to gene recombination, regulated gene expression using the tetracycline-controlled transactivator and reverse tetracycline-controlled transactivator systems, a powerful new means for modulating the activity of specific molecules, has been applied to CaMKII α and the opposing protein phosphatase calcineurin. Together with electro-physiological and behavioural evaluation of the engineered mutant animals, these genetic methodologies have helped gain insight into the molecular mechanisms of plasticity and memory. Further technical developments are, however, awaited for an even higher level of finesse.

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