Evidence map›Paper›PMID 11306653›Full record

ArticleThe Journal of physiology2001

Calcium influx-independent depression of transmitter release by 5-HT at lamprey spinal cord synapses.

M Takahashi, R Freed, T Blackmer, S Alford

Abstract read
In one paragraph

Article in The Journal of physiology, 2001. 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
–field-weighted citation impact
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.

  1. Article
  2. Single Calcium Channel Nanodomains Drive Presynaptic Calcium Entry at Lamprey Reticulospinal Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  3. Synaptic Integration of Subquantal Neurotransmission by Colocalized G Protein-Coupled Receptors in Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Modulation of neurotransmission by GPCRs is dependent upon the microarchitecture of the primed vesicle complex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  12. Article
  13. Review
  14. Article
  15. Presynaptic G-protein-coupled receptors dynamically modify vesicle fusion, synaptic cleft glutamate concentrations, and motor behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  16. Article
  17. Presynaptic G-protein-coupled receptors regulate synaptic cleft glutamate via transient vesicle fusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  18. G protein betagamma-subunits activated by serotonin mediate presynaptic inhibition by regulating vesicle fusion properties.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  19. Article
  20. Article
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

4 authors.

M TakahashiDepartment of Physiology, Northwestern University Medical School, Chicago, IL 60611, USA.
R Freed
T Blackmer
S Alford

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The mechanisms by which 5-hydroxytryptamine (5-HT) depresses transmitter release from lamprey reticulospinal axons were investigated. These axons make glutamatergic synapses onto spinal ventral horn neurons. 5-HT reduces release at these synapses, yet the mechanisms remain unclear. 2. Excitatory postsynaptic currents (EPSCs) evoked by stimulation of reticulospinal axons were recorded in ventral horn neurons. 5-HT depressed the EPSCs in a dose-dependent manner with an apparent Km of 2.3 microM. 3. To examine the presynaptic effect of 5-HT, electrophysiological and optical recordings were made from presynaptic axons. Action potentials evoked Ca(2+) transients in the axons loaded with a Ca(2+)-sensitive dye. 5-HT slightly reduced the Ca(2+) transient. 4. A third-power relationship between Ca(2+) entry and transmitter release was determined. However, presynaptic Ca(2+) currents were unaffected by 5-HT. 5. Further, in the presence of a K(+) channel blocker, 4-aminopyridine (4-AP), 5-HT left unaltered the presynaptic Ca(2+) transient, ruling out the possibility of its direct action on presynaptic Ca(2+) current. 5-HT activated a 4-AP-sensitive current with a reversal potential of -95 mV in these axons. 6. The basal Ca(2+) concentration did not affect 5-HT-mediated inhibition of release. Although 5-HT caused a subtle reduction in resting axonal [Ca(2+)]i, synaptic responses recorded during enhanced resting [Ca(2+)]i, by giving stimulus trains, were equally depressed by 5-HT. 7. 5-HT reduced the frequency of TTX-insensitive spontaneous EPSCs at these synapses, but had no effect on their amplitude. We propose a mechanism of inhibition for transmitter release by 5-HT that is independent of presynaptic Ca(2+) entry.

Indexed as

4-AminopyridineAction PotentialsAnimalsAxonsCalciumElectrophysiologyExcitatory Amino Acid AntagonistsGlutamic AcidLampreysMotor NeuronsNeurotransmitter AgentsPresynaptic TerminalsSerotoninSpinal CordSynapsesSynaptic Transmission4-AminopyridineCalciumExcitatory Amino Acid AntagonistsGlutamic AcidNeurotransmitter AgentsSerotonin

Identifiers

PMID11306653
PMCPMC2278557

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.