Mineralocorticoid receptors are indispensable for nongenomic modulation of hippocampal glutamate transmission by corticosterone.

By H. Karst, S. Berger, Marc Turiault, F. Tronche, G. Schütz, Marian Joëls. Proceedings of the National Academy of Sciences of the United States of America, 2005

797 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Endocrinology, Diabetes and Metabolism, Social Psychology

View Paper: https://www.semanticscholar.org/paper/092c9c4c6a45d2935b1fec79af778cab609d2b41

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Citations in the corpus

The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007, background): “We have found that rats given 2 minutes of cat exposure immediately before minimal water maze training demonstrated strong spatial memory 24 hours later (Figure 4(a)).”
11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action. (2013, background): “Moreover, a very short-term (1 h) effect of 11 -HSD1 inhibition on cognition in young rats has been reported (474); while the mechanisms are unclear, this raises again the intriguing possibility of rapid cognitive actions possibly mediated via membrane-associated corticosteroid receptors (337).”
Long-term depression in the CNS (2010, background): “, an effect that is mediated by corticosterone release and increased extracellular glutamate concentrations in the hippocampu”
Neurobiological and Systemic Effects of Chronic Stress (2017, background): “Indeed, corticosterone acts directly via membrane associated mineralocorticoid receptors (MR) and GR to cause glutamate release.(26,43,44) Blocking N-methyl-D-aspartate (NMDA) receptors and interfering with excitatory stimulation of ion channels blocks stress-induced dendritic remodeling, as also do”
Stress and Memory: Behavioral Effects and Neurobiological Mechanisms (2007, background): “[74] have recently reported that stress levels of corticosterone, by interacting with the mineralocorticoid receptor (MR), can rapidly enhance the frequency of miniature excitatory postsynaptic potentials in hippocampal CA1 pyramidal neurons and to reduced paired-pulse facilitation.”
The stressed synapse: the impact of stress and glucocorticoids on glutamate transmission (2011, methodology): “In different studies using patch-clamp recordings, application of 100 nM corticosterone (which is the major glucocorticoid in rodents) to hippocampal slices rapidly enhanced the frequency of miniature excitatory postsynaptic potentials in CA1 pyramidal neurons and reduced paired-pulse facilitation (”
Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators. (2008, background): “…receptors) receptor by genetic means has revealed that MR are required for nongenomic regulation of glutamatergic transmission by glucocorticoids (Karst et al., 2005), a phenomenon that involved glucocorticoid enhancement of extracellular levels of glutamate (Venero and Borrell, 1999) that plays…”
Towards a glutamate hypothesis of depression (2011, background): “…have been substantially confirmed by more recent works that used different methodologies measuring exocytotic release of glutamate (Cazakoff and Howland, 2010; Hascup et al., 2010; Karst et al., 2005; Musazzi et al., 2010; Reznikov et al., 2007; Satoh and Shimeki, 2010; Wang and Wang, 2009).”