ArticleMolecules and cells2011
State-dependent disruption of short-term facilitation due to overexpression of the apPDE4 supershort form in Aplysia.
Article in Molecules and cells, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Specific Expression of Aplysia Phosphodiesterase 4 in Bag Cells Revealed by in situ Hybridization Analysis.Experimental neurobiology · 2015Article
- Intracellular membrane association of the Aplysia cAMP phosphodiesterase long and short forms via different targeting mechanisms.The Journal of biological chemistry · 2014Article
- Learning-related synaptic growth mediated by internalization of Aplysia cell adhesion molecule is controlled by membrane phosphatidylinositol 4,5-bisphosphate synthetic pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
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 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphodiesterases (PDEs) play important roles in synaptic plasticity by regulating cAMP signaling in various organisms. The supershort, short, and long forms of Aplysia PDE4 (apPDE4) have been cloned, and the long form has been shown to play a crucial role in 5- hydroxytryptamine (5-HT)-induced synaptic plasticity in Aplysia. To address the role of the supershort form in 5-HT-induced synaptic plasticity in Aplysia, we overexpressed the apPDE4 supershort form in Aplysia sensory neurons. Consequently, 5-HT-induced hyperexcitability and short-term facilitation in nondepressed synapses were blocked. However, the supershort form did not inhibit 5-HT-induced short-term facilitation in highly depressed synapses. These results show that the supershort form plays an important role in 5-HT-induced synaptic plasticity and disrupts it mainly by impairing cAMP signaling in Aplysia.
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.