Trace fear conditioning involves hippocampal α5 GABAA receptors
By F. Crestani, R. Keist, J. Fritschy, Dietmar Benke, Kaspar E. Vogt, L. Prut, H. Blüthmann, H. Möhler, Uwe Rudolph. Proceedings of the National Academy of Sciences of the United States of America, 2002
519 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d1eee614675edbf6d3ab5daca2ba4fbcca18da4c
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In Cellular and Molecular Neuroscience
In Cognitive Neuroscience
- Richard W. Olsen
- W. Sieghart
- István Módy
- S. Brickley
- U. Rudolph
- M. Fanselow
- Z. Nusser
- Nicholas P. Franks
In Molecular Biology
Citations in the corpus
- Molecular and neuronal substrates for general anaesthetics (2004, background): “, whereas the myorelaxant action of diazepam is mediated by α2-, α3- and α5-containing GABA A receptor”
- Synaptic and nonsynaptic localization of GABAA receptors containing the α5 subunit in the rat brain (2006, methodology): “These results support the notion that 5- GABAARs are not exclusively localized extrasynaptically in a diffuse way, as proposed by others (Brunig et al., 2002; Crestani et al., 2002).”
- Trace fear conditioning is enhanced in mice lacking the δ subunit of the GABAA receptor (2005, background): “For example, recent experiments on GABAAR mutants ( 5 and 2) found enhanced trace but normal delay conditioning (Crestani et al. 1999, 2002).”
- An inverse agonist selective for α5 subunit-containing GABAA receptors improves encoding and recall but not consolidation in the Morris water maze (2006, background): “In accordance, reduced expression of α5 subunit-containing GABAA receptors has been reported to be associated with facilitation of aspects of cognition (Collinson et al. 2002; Crestani et al. 2002) and has resulted in these receptors to become a putative target for subtypeselective inverse agonists ”
- Tonic Inhibitory Control of Dentate Gyrus Granule Cells by α5-Containing GABAA Receptors Reduces Memory Interference (2015, background): “Previous studies have shown that the reduction of tonic inhibition through global manipulations can enhance trace fear conditioning (Collinson et al., 2002; Crestani et al., 2002; Yee et al., 2004; Wiltgen et al., 2005; Moore et al., 2010).”
- GABAA Receptors: Subtypes Provide Diversity of Function and Pharmacology (2008, unknown): “The a5bg2 receptors seem to influence learning and memory, shown by improved spatial memory in mice with knockout of a5 subunits (Collinson et al., 2002), and improved trace fear conditioning in the point-mutated a5 knock-in mouse (Crestani et al., 2002).”
- International Union of Pharmacology. LXX. Subtypes of γ-Aminobutyric AcidA Receptors: Classification on the Basis of Subunit Composition, Pharmacology, and Function. Update (2008, background): “…spatial memory in mice with knockout of (cid:2) 5 subunits (Collinson et al., 2000), and trace fear conditioning was facilitated in the point-mutated (cid:2) 5 knockin which unex-plainedly showed major (cid:2) 5 subunit knockdown in the CA1 region (Crestani et al., 2002; Rudolph and Mo¨hler, 2004).”
- Variations on an inhibitory theme: phasic and tonic activation of GABAA receptors (2005, background): “In hippocampal pyramidal cells, the α5 subunit (which probably forms α 5 β 3 γ 2 receptors) shows diffuse surface labelling at the light microscopic level without detectable synaptic clustering, as judged by the lack of co-localization with gephyri”
- Extrasynaptic GABAA receptors: Their function in the CNS and implications for disease (2012, background): “First, mice with a partial or full deficit of a5-GABAARs show improved performance in associative learning and memory tasks (Collinson et al., 2002; Crestani et al., 2002; Yee et al., 2004), with only a minimal deficit in memory for object location (Prut et al., 2010).”
- Beyond classical benzodiazepines: Novel therapeutic potential of GABAA receptor subtypes (2011, background): “Histidine-to-arginine point mutations at a conserved residue in the α1, α2, α3 or α5 subunit abolish binding of diazepam, whereas the action of the physiological neurotransmitter GABA is preserve”