Evidence map›Paper›PMID 15626456›Full record

ReviewPharmacology & therapeutics2005

Modulation of neurotransmitter release by the second messenger-activated protein kinases: implications for presynaptic plasticity.

A G Miriam Leenders, Zu-Hang Sheng

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

86 citing papers in PubMed, 184 citations in OpenAlex.

  1. Article
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  4. BK channels mediate a presynaptic form of mGluR-LTD in the neonatal hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025
    Review
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  19. Eupafolin Suppresses P/Q-Type CaBiomolecules & therapeutics · 2021
    Article
  20. Article

26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

A G Miriam LeendersSynaptic Function Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 35, Room 3B203, 35 Convent Drive, Bethesda, MD 20892-3701, USA.
Zu-Hang Sheng
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · US

Funding

Transport and regulation of presynaptic release machineryZIANS002946 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2009 to 2025
$25.6M
Transport and regulation of presynaptic release machineryZ01NS002946 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 1997 to 2008
$2.1M
NINDS NIH HHS Z01 NS002946-09
6 · The paper itself

Abstract

Activity-dependent modulation of synaptic function and structure is emerging as one of the key mechanisms underlying synaptic plasticity. Whereas over the past decade considerable progress has been made in identifying postsynaptic mechanisms for synaptic plasticity, the presynaptic mechanisms involved have remained largely elusive. Recent evidence implicates that second messenger regulation of the protein interactions in synaptic vesicle release machinery is one mechanism by which cellular events modulate synaptic transmission. Thus, identifying protein kinases and their targets in nerve terminals, particularly those functionally regulated by synaptic activity or intracellular [Ca2+], is critical to the elucidation of the molecular mechanisms underlying modulation of neurotransmitter release and presynaptic plasticity. The phosphorylation and dephosphorylation states of synaptic proteins that mediate vesicle exocytosis could regulate the biochemical pathways leading from synaptic vesicle docking to fusion. However, functional evaluation of the activity-dependent phosphorylation events for modulating presynaptic functions still represents a considerable challenge. Here, we present a brief overview of the data on the newly identified candidate targets of the second messenger-activated protein kinases in the presynaptic release machinery and discuss the potential impact of these phosphorylation events in synaptic strength and presynaptic plasticity.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein KinasesHumansNeuronal PlasticityNeurotransmitter AgentsProtein Kinase CProtein KinasesReceptors, PresynapticSecond Messenger SystemsSynapsinsCalcium-Calmodulin-Dependent Protein KinasesNeurotransmitter AgentsProtein Kinase CProtein KinasesReceptors, PresynapticSynapsins

Identifiers

PMID15626456
PMCPMC1804289
OpenAlexW2028793193

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.