Evidence map›Paper›PMID 25319700›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Presynaptic T-type Ca2+ channels modulate dendrodendritic mitral-mitral and mitral-periglomerular connections in mouse olfactory bulb.

Adam Fekete, Jamie Johnston, Kerry R Delaney

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023
    Article
  3. Review
  4. Intracellular Calcium Responses Encode Action Potential Firing in Spinal Cord Lamina I Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  5. Article
  6. Review
  7. Activity-dependent increases in [CaJournal of neurophysiology · 2017
    Article
  8. Adenosine AFrontiers in cellular neuroscience · 2017
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. 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

3 authors at 2 institutions in 2 countries.

Adam FeketeDepartment of Biology, University of Victoria, Victoria, British Columbia, V8W 2Y2, Canada, Program in Neurosciences and Mental Health, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada, and.
Jamie JohnstonDepartment of Biology, University of Victoria, Victoria, British Columbia, V8W 2Y2, Canada, Sussex Neuroscience, School of Life Sciences, University of Sussex, Falmer, Brighton, BN1 9QG, United Kingdom.
Kerry R DelaneyDepartment of Biology, University of Victoria, Victoria, British Columbia, V8W 2Y2, Canada, kdelaney@uvic.ca.
University of Victoria · CASickKids Foundation · CA

Funding

Canadian Institutes of Health Research MOP 86473
6 · The paper itself

Abstract

Mitral cells express low-voltage activated Cav3.3 channels on their distal apical tuft dendrites (McKay et al., 2006; Johnston and Delaney, 2010). They also discharge Na(+)-dependent dendritic action potentials and release glutamate from these dendrites. Around resting membrane potentials, between -65 and -50 mV, Cav3.x channels are a primary determinant of cytoplasmic [Ca(2+)]. In this study using C57 mice, we present evidence that subthreshold Cav3.x-mediated Ca(2+) influx modulates action potential evoked transmitter release and directly drives asynchronous release from distal tuft dendrites. Presynaptic hyperpolarization and selective block of Cav3.x channels with Z941 (Tringham et al., 2012) reduce mitral-to-mitral EPSP amplitude, increase the coefficient of variation of EPSPs, and increase paired-pulse ratios, consistent with a reduced probability of transmitter release. Both hyperpolarization and Cav3.x channel blockade reduce steady-state cytoplasmic [Ca(2+)] in the tuft dendrite without reducing action potential evoked Ca(2+) influx, suggesting that background [Ca(2+)] modulates evoked release. We demonstrate that Cav3.x-mediated Ca(2+) influx from even one mitral cell at membrane potentials between -65 and -50 mV is sufficient to produce feedback inhibition from periglomerular neurons. Deinactivation of Cav3.x channels by hyperpolarization increases T-type Ca(2+) influx upon repolarization and increases feedback inhibition to produce subthreshold modulation of the mitral-periglomerular reciprocal circuit.

Indexed as

Action PotentialsAnimalsCalcium Channels, T-TypeCaveolin 3DendritesExcitatory Postsynaptic PotentialsFemaleMaleMembrane PotentialsMiceMice, Inbred C57BLNeural InhibitionOlfactory BulbOlfactory PathwaysOrgan Culture TechniquesPresynaptic TerminalsCalcium Channels, T-TypeCav3 protein, mouseCaveolin 3asynchronous releasebasal Ca2+ leveldendrodendritic releaseolfactory mitral cellssubthreshold potentialT-channel (Cav3)

Identifiers

PMID25319700
PMCPMC6705286
OpenAlexW1988329215

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.