ArticleScientific reports2019
Neurotropic and modulatory effects of insulin-like growth factor II in Aplysia.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Pattern detection in the TGFβ cascade controls the induction of long-term synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- IGF2 in memory, neurodevelopmental disorders, and neurodegenerative diseases.Trends in neurosciences · 2023Review
- Insulin-like growth factor 2 (IGF-2) rescues social deficits in NLG3Frontiers in cellular neuroscience · 2023Article
- Cell Cycle Re-entry in the Nervous System: From Polyploidy to Neurodegeneration.Frontiers in cell and developmental biology · 2021Review
- Effect of photoperiod and light intensity on learning ability and memory formation of the pond snail Lymnaea stagnalis.Invertebrate neuroscience : IN · 2020Article
- Postsynaptic effects ofLearning & memory (Cold Spring Harbor, N.Y.) · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Insulin-like growth factor II (IGF2) enhances memory in rodents via the mannose-6-phosphate receptor (M6PR), but the underlying mechanisms remain poorly understood. We found that human IGF2 produces an enhancement of both synaptic transmission and neurite outgrowth in the marine mollusk Aplysia californica. These findings were unexpected since Aplysia lack the mammal-specific affinity between insulin-like ligands and M6PR. Surprisingly, this effect was observed in parallel with a suppression of neuronal excitability in a well-understood circuit that supports several temporally and mechanistically distinct forms of memory in the defensive withdrawal reflex, suggesting functional coordination between excitability and memory formation. We hypothesize that these effects represent behavioral adaptations to feeding that are mediated by the endogenous Aplysia insulin-like system. Indeed, the exogenous application of a single recombinant insulin-like peptide cloned from the Aplysia CNS cDNA replicated both the enhancement of synaptic transmission, the reduction of excitability, and promoted clearance of glucose from the hemolymph, a hallmark of bona fide insulin action.
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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.