Evidence map›Paper›PMID 16611817›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Requirement of Akt to mediate long-term synaptic depression in Drosophila.

Hui-Fu Guo, Yi Zhong

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Gene model for the ortholog ofbioRxiv : the preprint server for biology · 2025
    Article
  3. Alterations of RNA-binding proteinFrontiers in molecular neuroscience · 2022
    Article
  4. Drosophila eugracilis - Akt.microPublication biology · 2022
    Article
  5. Article
  6. Article
  7. Machine Learning Analysis IdentifiesG3 (Bethesda, Md.) · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. AKT/GSK3 signaling pathway and schizophrenia.Frontiers in molecular neuroscience · 2012
    Article
  14. PI3 kinase signaling is involved in Abeta-induced memory loss in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  15. Two forms of long-term depression in a polysynaptic pathway in the leech CNS: one NMDA receptor-dependent and the other cannabinoid-dependent.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2009
    Article
  16. Article
  17. Distinctive roles of different beta-amyloid 42 aggregates in modulation of synaptic functions.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Hui-Fu GuoCold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
Yi Zhong
Cold Spring Harbor Laboratory · US

Funding

RAS/RAF PATHWAY IN NEUROTRANSMISSION IN DROSOPHILAR01NS034779 · NINDS · COLD SPRING HARBOR LABORATORY · PI ZHONG, YI · 1996 to 2003
$1.2M
NINDS NIH HHS 5R01-NS34779-08
6 · The paper itself

Abstract

Drosophila larval neuromuscular junction (NMJ) is a well established preparation enabling quantitative analyses of synaptic physiology at identifiable synapses. Here, we report the first characterization of synaptic long-term depression (LTD) at the Drosophila NMJ. LTD can be reliably induced by specific patterns of tetanic stimulation, and the level of LTD depends on both stimulus frequency and Ca2+ concentration. We provide evidence that LTD is likely a result of presynaptic changes. Through screening of targeted mutants with defects in memory or signal transduction pathways, we found that LTD is strongly reduced in the akt mutants. This defect can be rescued by acutely induced expression of the normal akt transgene, suggesting that altered LTD is not attributable to developmental abnormalities and that Akt is critical for the induction of LTD. Our study also indicates that the molecular mechanisms of LTD are distinct from that of short-term synaptic plasticity, because akt mutants showed normal short-term facilitation and posttetanic potentiation, whereas LTD was unaffected in mutants that exhibit defective short-term synaptic plasticity, such as dunce and rutabaga. The characterization of LTD allows genetic analysis of the molecular mechanisms of long-term synaptic plasticity in Drosophila and provides an additional assay for studying functions of genes pertaining to synaptic and behavioral plasticity.

Indexed as

AnimalsCalciumCalcium ChlorideDrosophilaLarvaLeukotriene D4Neuromuscular JunctionProto-Oncogene Proteins c-aktCalciumCalcium ChlorideLeukotriene D4Proto-Oncogene Proteins c-akt

Identifiers

PMID16611817
PMCPMC6673878
OpenAlexW2072381888

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.