ArticlePloS one2009
Regulation of hippocampal and behavioral excitability by cyclin-dependent kinase 5.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Cyclin-dependent kinase 5 (CDK5) inhibitors in Parkinson disease.Journal of cellular and molecular medicine · 2024Review
- Systemic Administration of a Brain Permeable Cdk5 Inhibitor Alters Neurobehavior.Frontiers in pharmacology · 2022Article
- Behavioral Deficits in Mice with Postnatal Disruption ofCerebral cortex communications · 2021Article
- Computational Simulations Identify Pyrrolidine-2,3-Dione Derivatives as Novel Inhibitors of Cdk5/p25 Complex to Attenuate Alzheimer's Pathology.Journal of clinical medicine · 2019Article
- Cyclin-dependent kinase 5 mediates pleiotrophin-induced endothelial cell migration.Scientific reports · 2018Article
- Synaptic roles of cyclin-dependent kinase 5 & its implications in epilepsy.The Indian journal of medical research · 2017Review
- Neuroprotective Mechanisms Mediated by CDK5 Inhibition.Current pharmaceutical design · 2016Review
- Article
- Beneficial effects of polydatin on learning and memory in rats with chronic ethanol exposure.International journal of clinical and experimental pathology · 2015Article
- Forebrain-specific deletion of Cdk5 in pyramidal neurons results in mania-like behavior and cognitive impairment.Neurobiology of learning and memory · 2013Article
- Functional and mechanistic exploration of an adult neurogenesis-promoting small molecule.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Schizophrenia is associated with dysregulation of a Cdk5 activator that regulates synaptic protein expression and cognition.Brain : a journal of neurology · 2011Article
- The role of Cdk5 in cognition and neuropsychiatric and neurological pathology.Brain research bulletin · 2011Review
- Cdk5 is required for memory function and hippocampal plasticity via the cAMP signaling pathway.PloS one · 2011Article
- Attention-deficit/hyperactivity phenotype in mice lacking the cyclin-dependent kinase 5 cofactor p35.Biological psychiatry · 2010Article
- Involvement of cyclin-dependent kinase-like 2 in cognitive function required for contextual and spatial learning in mice.Frontiers in behavioral neuroscience · 2010Article
- Getting Excited Through Cyclin: A Role for Endothelial Cdk5 Signaling in Hippocampal Hyperexcitability.Epilepsy currentsArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Cyclin-dependent kinase 5 (Cdk5) is a proline-directed serine/threonine kinase that has been implicated in learning, synaptic plasticity, neurotransmission, and numerous neurological disorders. We previously showed that conditional loss of Cdk5 in adult mice enhanced hippocampal learning and plasticity via modulation of calpain-mediated N-methyl-D-aspartic acid receptor (NMDAR) degradation. In the present study, we characterize the enhanced synaptic plasticity and examine the effects of long-term Cdk5 loss on hippocampal excitability in adult mice. Field excitatory post-synaptic potentials (fEPSPs) from the Schaffer collateral CA1 subregion of the hippocampus (SC/CA1) reveal that loss of Cdk5 altered theta burst topography and enhanced post-tetanic potentiation. Since Cdk5 governs NMDAR NR2B subunit levels, we investigated the effects of long-term Cdk5 knockout on hippocampal neuronal excitability by measuring NMDAR-mediated fEPSP magnitudes and population-spike thresholds. Long-term loss of Cdk5 led to increased Mg(2+)-sensitive potentials and a lower threshold for epileptiform activity and seizures. Biochemical analyses were performed to better understand the role of Cdk5 in seizures. Induced-seizures in wild-type animals led to elevated amounts of p25, the Cdk5-activating cofactor. Long-term, but not acute, loss of Cdk5 led to decreased p25 levels, suggesting that Cdk5/p25 may be activated as a homeostatic mechanism to attenuate epileptiform activity. These findings indicate that Cdk5 regulates synaptic plasticity, controls neuronal and behavioral stimulus-induced excitability and may be a novel pharmacological target for cognitive and anticonvulsant therapies.
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Registered trials
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.