Evidence map›Paper›PMID 11356859›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Presynaptic Ca2+ channels and neurotransmitter release at the terminal of a mouse cortical neuron.

J Qian, J L Noebels

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Article
  3. Deletion of the P/Q-Type Calcium Channel from Serotonergic Neurons Drives Male Aggression in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  4. Article
  5. (2R,6R)-hydroxynorketamine rapidly potentiates hippocampal glutamatergic transmission through a synapse-specific presynaptic mechanism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Article
  6. Article
  7. Nanomachinery Organizing Release at Neuronal and Ribbon Synapses.International journal of molecular sciences · 2019
    Review
  8. MAP6 interacts with Tctex1 and CaThe European journal of neuroscience · 2017
    Article
  9. Article
  10. Isolated P/Q Calcium Channel Deletion in Layer VI Corticothalamic Neurons Generates Absence Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  11. Review: CaThe open neurology journal · 2016
    Article
  12. LRRK2 Regulates Voltage-Gated Calcium Channel Function.Frontiers in molecular neuroscience · 2016
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. P/Q-type calcium channel modulators.British journal of pharmacology · 2012
    Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

J QianDepartment of Neurology, Baylor College of Medicine, Houston, Texas 77030, USA.
J L Noebels
Baylor College of Medicine · US

Funding

PLASTICITY IN DEVELOPING EPILEPTIC BRAINR01NS029709 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI NOEBELS, JEFFREY · 1991 to 2025
$9.1M
NINDS NIH HHS NS29709NINDS NIH HHS R01 NS029709
6 · The paper itself

Abstract

Regional variation in synaptic efficacy is an important determinant of associative processing as information flows through major circuits of the brain. The perforant path is the principal route of entry from cortex to the hippocampus and contains the first synapse in the cortical-hippocampal projection pathway. We used optical imaging techniques to analyze presynaptic Ca(2+) entry and neurotransmitter release at synapses in the medial perforant path linking stellate neurons located in layer II of the entorhinal cortex to granule cells in the dentate gyrus. Similar to other excitatory central synapses, the relationship between neurotransmitter release and the amount of Ca(2+) influx can be best described by a Hill equation with a Hill coefficient of 3.5. Our Ca(2+) channel toxin studies indicate that P/Q-type channels are the predominant Ca(2+) source triggering neurotransmitter release in this pathway, as shown by a potent inhibition of Ca(2+) entry and synaptic transmission by the P/Q-type channel blocker omega-agatoxin IVA. However, compared with the downstream hippocampal pyramidal neuron CA3-CA1 synapse, neurotransmitter release was less sensitive to the N-type Ca(2+) channel blocker omega-conotoxin GVIA, although the amount of N-type Ca(2+) current is comparable. The contribution of N-type channels to neurotransmitter release approximates that found at the CA3-CA1 synapse when tested under lower [Ca(2+)](o), which effectively reduces the size of the Ca(2+) microdomain surrounding each channel. These results suggest that P/Q-type channels are more closely associated with release machinery then N-type channels at this synapse and that cooperativity differences for each channel subtype may characterize variations in signaling at central synapses.

Indexed as

AnimalsCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeDentate GyrusEntorhinal CortexExcitatory Postsynaptic PotentialsFluorescent DyesIn Vitro TechniquesMiceModels, NeurologicalNeuronsNeurotransmitter AgentsCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeFluorescent DyesNeurotransmitter Agents

Identifiers

PMID11356859
PMCPMC6762720
OpenAlexW2133680532

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.