ArticleProceedings of the National Academy of Sciences of the United States of America2015
Network compensation of cyclic GMP-dependent protein kinase II knockout in the hippocampus by Ca2+-permeable AMPA receptors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
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- Phosphorylation of the AMPA receptor subunit GluA1 regulates clathrin-mediated receptor internalization.Journal of cell science · 2021Article
- Loss of cGMP-dependent protein kinase II alters ultrasonic vocalizations in mice, a model for speech impairment in human microdeletion 4q21 syndrome.Neuroscience letters · 2021Article
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- Evaluation of the Neuroprotective Effect of Sirt3 in Experimental Stroke.Translational stroke research · 2019Article
- AKAP150 Palmitoylation Regulates Synaptic Incorporation of CaCell reports · 2018Article
- The Phosphodiesterase 9 Inhibitor PF-04449613 Promotes Dendritic Spine Formation and Performance Improvement after Motor Learning.Developmental neurobiology · 2018Article
- HIV induces synaptic hyperexcitation via cGMP-dependent protein kinase II activation in the FIV infection model.PLoS biology · 2018Article
- Activation of cyclic GMP-dependent protein kinase blocks alcohol-mediated cell death and calcium disruption in cerebellar granule neurons.Neuroscience letters · 2018Article
- Control of Homeostatic Synaptic Plasticity by AKAP-Anchored Kinase and Phosphatase Regulation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Enhanced synaptic plasticity and spatial memory in female but not male FLRT2-haplodeficient mice.Scientific reports · 2018Article
- Translocator protein (18 kDa): an update on its function in steroidogenesis.Journal of neuroendocrinology · 2018Review
- The Role of Calcium-Permeable AMPARs in Long-Term Potentiation at Principal Neurons in the Rodent Hippocampus.Frontiers in synaptic neuroscience · 2018Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Gene knockout (KO) does not always result in phenotypic changes, possibly due to mechanisms of functional compensation. We have studied mice lacking cGMP-dependent kinase II (cGKII), which phosphorylates GluA1, a subunit of AMPA receptors (AMPARs), and promotes hippocampal long-term potentiation (LTP) through AMPAR trafficking. Acute cGKII inhibition significantly reduces LTP, whereas cGKII KO mice show no LTP impairment. Significantly, the closely related kinase, cGKI, does not compensate for cGKII KO. Here, we describe a previously unidentified pathway in the KO hippocampus that provides functional compensation for the LTP impairment observed when cGKII is acutely inhibited. We found that in cultured cGKII KO hippocampal neurons, cGKII-dependent phosphorylation of inositol 1,4,5-trisphosphate receptors was decreased, reducing cytoplasmic Ca(2+) signals. This led to a reduction of calcineurin activity, thereby stabilizing GluA1 phosphorylation and promoting synaptic expression of Ca(2+)-permeable AMPARs, which in turn induced a previously unidentified form of LTP as a compensatory response in the KO hippocampus. Calcineurin-dependent Ca(2+)-permeable AMPAR expression observed here is also used during activity-dependent homeostatic synaptic plasticity. Thus, a homeostatic mechanism used during activity reduction provides functional compensation for gene KO in the cGKII KO hippocampus.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.