ArticleNature2013
PKM-ζ is not required for hippocampal synaptic plasticity, learning and memory.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 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
181 citing papers in PubMed, 317 citations in OpenAlex.
- Molecular architects of memory: BDNF/TrkB signaling and trafficking in neuronal plasticity and memory.Molecular psychiatry · 2026Review
- Article
- Persistently Increased Expression of PKMzeta and Unbiased Gene Expression Profiles Identify Hippocampal Molecular Traces of a Long-Term Active Place Avoidance Memory and "Shadow" Proteins.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- PKM ζ-PKC ι / λ double-knockout demonstrates atypical PKC is crucial for the persistence of hippocampal LTP and spatial memory.bioRxiv : the preprint server for biology · 2026Article
- PKMζ in the prefrontal cortex alters cocaine cue-induced reinstatement in a sex-specific manner.Psychopharmacology · 2026Article
- PKMζ is necessary for long-term depression and long-term potentiation in the medial prefrontal cortex.The Journal of physiology · 2026Article
- Persistently increased expression of PKMzeta and unbiased gene expression profiles identify hippocampal molecular traces of a long-term active place avoidance memory and 'shadow' proteins.bioRxiv : the preprint server for biology · 2025Article
- Article
- A revised view of the role of CaMKII in learning and memory.Nature neuroscience · 2025Review
- PKMζ drives spatial memory reconsolidation but not maintenance.Frontiers in synaptic neuroscience · 2025Article
- PKMζ alters oxycodone-taking in a dose- and sex-dependent manner.Addiction neuroscience · 2024Article
- Active forgetting and neuropsychiatric diseases.Molecular psychiatry · 2024Review
- KIBRA anchoring the action of PKMζ maintains the persistence of memory.Science advances · 2024Article
- KIBRA repairs synaptic plasticity and promotes resilience to tauopathy-related memory loss.The Journal of clinical investigation · 2024Article
- Cationic peptides erase memories by removing synaptic AMPA receptors through endophilin-mediated endocytosis.Research square · 2023Article
- Photoactivated Protein Degrader for Optical Control of Synaptic Function.ACS chemical neuroscience · 2023Article
- PD-L1/PD-1 checkpoint pathway regulates hippocampal neuronal excitability and learning and memory behavior.Neuron · 2023Article
- Sex differences in pre- and post-synaptic glutamate signaling in the nucleus accumbens core.Biology of sex differences · 2023Article
- Karim Nader and the unification of memory erasure: PKMζ inhibition and reconsolidation blockade.Brain research bulletin · 2023Review
121 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Long-term potentiation (LTP), a well-characterized form of synaptic plasticity, has long been postulated as a cellular correlate of learning and memory. Although LTP can persist for long periods of time, the mechanisms underlying LTP maintenance, in the midst of ongoing protein turnover and synaptic activity, remain elusive. Sustained activation of the brain-specific protein kinase C (PKC) isoform protein kinase M-ζ (PKM-ζ) has been reported to be necessary for both LTP maintenance and long-term memory. Inhibiting PKM-ζ activity using a synthetic zeta inhibitory peptide (ZIP) based on the PKC-ζ pseudosubstrate sequence reverses established LTP in vitro and in vivo. More notably, infusion of ZIP eliminates memories for a growing list of experience-dependent behaviours, including active place avoidance, conditioned taste aversion, fear conditioning and spatial learning. However, most of the evidence supporting a role for PKM-ζ in LTP and memory relies heavily on pharmacological inhibition of PKM-ζ by ZIP. To further investigate the involvement of PKM-ζ in the maintenance of LTP and memory, we generated transgenic mice lacking PKC-ζ and PKM-ζ. We find that both conventional and conditional PKC-ζ/PKM-ζ knockout mice show normal synaptic transmission and LTP at Schaffer collateral-CA1 synapses, and have no deficits in several hippocampal-dependent learning and memory tasks. Notably, ZIP still reverses LTP in PKC-ζ/PKM-ζ knockout mice, indicating that the effects of ZIP are independent of PKM-ζ.
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.