ArticleNeurobiology of learning and memory2013
Forebrain-specific deletion of Cdk5 in pyramidal neurons results in mania-like behavior and cognitive impairment.
Article in Neurobiology of learning and memory, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Neuron-specific epigenetic repression ofbioRxiv : the preprint server for biology · 2026Article
- Transcriptomic Architecture of Weak Versus Strong Contextual Fear Extinction Learning Uncovers Extinction-Suppressive Role of TIA1.Biological psychiatry global open science · 2025Article
- Inhibition of Cdk5 in PV Neurons Reactivates Experience-Dependent Plasticity in Adult Visual Cortex.International journal of molecular sciences · 2021Article
- Activation of VGluT2-expressing neurons in the bed nuclei of the stria terminalis produces mouse manic-like behaviors.CNS neuroscience & therapeutics · 2021Article
- In vivo locus-specific editing of the neuroepigenome.Nature reviews. Neuroscience · 2020Review
- The Role of Cdk5 in Alzheimer's Disease.Molecular neurobiology · 2016Review
- MicroRNA-155 deletion reduces anxiety- and depressive-like behaviors in mice.Psychoneuroendocrinology · 2016Article
- Molecular Genetic Strategies in the Study of Corticohippocampal Circuits.Cold Spring Harbor perspectives in biology · 2015Review
- Loss of cyclin-dependent kinase 5 from parvalbumin interneurons leads to hyperinhibition, decreased anxiety, and memory impairment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Cdk5/p35 functions as a crucial regulator of spatial learning and memory.Molecular brain · 2014Article
- Cyclin-dependent kinase 5 in the ventral tegmental area regulates depression-related behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cyclin-dependent kinase 5 (Cdk5) is associated with synaptic plasticity and cognitive function. Previous reports have demonstrated that Cdk5 is necessary for memory formation, although others have reported Cdk5 conditional knockout mouse models exhibiting enhanced learning and memory. Furthermore, how Cdk5 acts in specific cell populations to affect behavior and cognitive outcomes remains unclear. Here we conduct a behavioral characterization of a forebrain-specific Cdk5 conditional knockout mouse model under the αCaMKII promoter, in which Cdk5 is ablated in excitatory pyramidal neurons of the forebrain. The Cdk5 conditional knockouts exhibit hyperactivity in the open field, reduced anxiety, and reduced behavioral despair. Moreover, the Cdk5 conditional knockouts also display impaired spatial learning in the Morris water maze and are severely impaired in contextual fear memory, which correspond to deficits in synaptic transmission. Remarkably, the hyperactivity of the Cdk5 conditional knockouts can be ameliorated by the administration of lithium chloride, an inhibitor of GSK3β signaling. Collectively, our data reveal that Cdk5 ablation from forebrain excitatory neurons results in deleterious effects on emotional and cognitive behavior and highlight a key role for Cdk5 in regulating the GSK3β signaling pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.