Evidence map›Paper›PMID 35533198›Full record

ArticlePLoS computational biology2022

Multiscale modeling of presynaptic dynamics from molecular to mesoscale.

Jonathan W Garcia, Thomas M Bartol, Terrence J Sejnowski

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ACognitive neurodynamics · 2024
    Article
  5. CellVis2: a conference on visualizing the molecular cell.Trends in biochemical sciences · 2024
    Article
  6. Review
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

3 authors at 1 institution in 1 country.

Jonathan W GarciaDivision of Biological Sciences, University of California San Diego, La Jolla, California, United States of America.ORCID 0000-0001-6811-0415
Thomas M BartolComputational Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, California, United States of America.
Terrence J SejnowskiDivision of Biological Sciences, University of California San Diego, La Jolla, California, United States of America.ORCID 0000-0002-0622-7391
Salk Institute for Biological Studies · US

Funding

TrainingP41GM103712 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FAEDER, JAMES · 2012 to 2021
$16.3M
Neurosciences Graduate Training ProgramT32NS061847 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Brenda L Bloodgood · 2008 to 2026
$7.7M
Howard Hughes Medical InstituteNIGMS NIH HHS P41 GM103712NINDS NIH HHS T32 NS061847
6 · The paper itself

Abstract

Chemical synapses exhibit a diverse array of internal mechanisms that affect the dynamics of transmission efficacy. Many of these processes, such as release of neurotransmitter and vesicle recycling, depend strongly on activity-dependent influx and accumulation of Ca2+. To model how each of these processes may affect the processing of information in neural circuits, and how their dysfunction may lead to disease states, requires a computationally efficient modelling framework, capable of generating accurate phenomenology without incurring a heavy computational cost per synapse. Constructing a phenomenologically realistic model requires the precise characterization of the timing and probability of neurotransmitter release. Difficulties arise in that functional forms of instantaneous release rate can be difficult to extract from noisy data without running many thousands of trials, and in biophysical synapses, facilitation of per-vesicle release probability is confounded by depletion. To overcome this, we obtained traces of free Ca2+ concentration in response to various action potential stimulus trains from a molecular MCell model of a hippocampal Schaffer collateral axon. Ca2+ sensors were placed at varying distance from a voltage-dependent calcium channel (VDCC) cluster, and Ca2+ was buffered by calbindin. Then, using the calcium traces to drive deterministic state vector models of synaptotagmin 1 and 7 (Syt-1/7), which respectively mediate synchronous and asynchronous release in excitatory hippocampal synapses, we obtained high-resolution profiles of instantaneous release rate, to which we applied functional fits. Synchronous vesicle release occurred predominantly within half a micron of the source of spike-evoked Ca2+ influx, while asynchronous release occurred more consistently at all distances. Both fast and slow mechanisms exhibited multi-exponential release rate curves, whose magnitudes decayed exponentially with distance from the Ca2+ source. Profile parameters facilitate on different time scales according to a single, general facilitation function. These functional descriptions lay the groundwork for efficient mesoscale modelling of vesicular release dynamics.

Indexed as

CalciumSynapsesAction PotentialsNeurotransmitter AgentsSynaptic TransmissionCalciumNeurotransmitter Agents

Identifiers

PMID35533198
PMCPMC9119629
OpenAlexW4229445722

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.