ArticleFrontiers in cellular neuroscience2014
Distinct roles of α- and βCaMKII in controlling long-term potentiation of GABAA-receptor mediated transmission in murine Purkinje cells.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 15 citations in OpenAlex.
- The Yin and Yang of GABAergic and Glutamatergic Synaptic Plasticity: Opposites in Balance by Crosstalking Mechanisms.Frontiers in synaptic neuroscience · 2022Review
- CaMKIIβ in Neuronal Development and Plasticity: An Emerging Candidate in Brain Diseases.International journal of molecular sciences · 2020Review
- Analysis of the CaMKIIα and β splice-variant distribution among brain regions reveals isoform-specific differences in holoenzyme formation.Scientific reports · 2018Article
- Non-canonical heterogeneous cellular distribution and co-localization of CaMKIIα and CaMKIIβ in the spinal superficial dorsal horn.Brain structure & function · 2018Article
- The molecular, temporal and region-specific requirements of the beta isoform of Calcium/Calmodulin-dependent protein kinase type 2 (CAMK2B) in mouse locomotion.Scientific reports · 2016Article
- Motor Learning and the Cerebellum.Cold Spring Harbor perspectives in biology · 2015Review
- Editorial: Plasticity of GABAergic synapses.Frontiers in cellular neuroscience · 2015Article
- Opposite regulation of inhibitory synaptic plasticity by α and β subunits of Ca(2+)/calmodulin-dependent protein kinase II.The Journal of physiology · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium/Calmodulin-dependent kinase type II (CaMKII) is essential for various forms of synaptic plasticity. The predominant α- and βCaMKII isoforms have both been shown to contribute to specific forms of plasticity at excitatory synapses, but little is known about their functions at inhibitory synapses. Here we investigated the role of both isoforms in long-term potentiation of the inhibitory molecular layer interneuron to Purkinje cell synapse (MLI-PC iLTP) upon climbing fiber (CF) stimulation. We demonstrate that deleting either the α- or βCaMKII isoform affected MLI-PC iLTP. In the presence of the PP2B blocker cyclosporin A, CF stimulation elicited iLTP in Camk2b (-) (/) (-) mice, but not in Camk2a (-) (/) (-) mice. Moreover, co-activation of the MLIs and CF suppressed iLTP in wild-type mice through activation of GABAB-receptors, whereas it evoked iLTP in Camk2b (-) (/) (-). This reversal of the effect of αCaMKII activity in Camk2b (-) (/) (-) mutants upon co-activation did not critically involve protein kinase A, but depended on calcium release from internal stores. Our results indicate that α- and βCaMKII isoforms in Purkinje cells can be differentially activated and serve distinct roles in controlling iLTP. We propose that the CaMKII holo-enzyme may be selectively activated by various GABAB-mediated pathways and that the presence of the βCaMKII isoform determines their impact on inhibitory plasticity.
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.