Evidence map›Paper›PMID 18171920›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Mutations in a Drosophila alpha2delta voltage-gated calcium channel subunit reveal a crucial synaptic function.

Dion K Dickman, Peri T Kurshan, Thomas L Schwarz

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing 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

58 citing papers in PubMed.

  1. Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Review
  3. Review
  4. CaeLife · 2024
    Article
  5. Article
  6. CabioRxiv : the preprint server for biology · 2024
    Article
  7. The importance of cache domains in αChannels (Austin, Tex.) · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Auxiliary α2δ1 and α2δ3 Subunits of Calcium Channels Drive Excitatory and Inhibitory Neuronal Network Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  13. Electrophysiological Profile RemodelingFrontiers in cellular neuroscience · 2020
    Article
  14. The calcium channel subunit αNature communications · 2019
    Article
  15. Deletion of the CaFrontiers in cellular neuroscience · 2019
    Article
  16. Article
  17. Review
  18. Review
  19. Electrophysiological analysis of synaptic transmission in Drosophila.Wiley interdisciplinary reviews. Developmental biology · 2017
    Review
  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

3 authors.

Dion K DickmanF. M. Kirby Neurobiology Center, Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Peri T Kurshan
Thomas L Schwarz

Funding

Genetics of New Synaptic Components and Their FunctionsR01NS041062 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI SCHWARZ, THOMAS L. · 2000 to 2017
$8.5M
NINDS NIH HHS R01 NS041062
6 · The paper itself

Abstract

Voltage-dependent calcium channels regulate many aspects of neuronal biology, including synaptic transmission. In addition to their alpha1 subunit, which encodes the essential voltage gate and selective pore, calcium channels also contain auxiliary alpha2delta, beta, and gamma subunits. Despite progress in understanding the biophysical properties of calcium channels, the in vivo functions of these auxiliary subunits remain unclear. We have isolated mutations in the gene encoding an alpha2delta calcium channel subunit (d alpha2delta-3) using a forward genetic screen in Drosophila. Null mutations in this gene are embryonic lethal and can be rescued by expression in the nervous system, demonstrating that the essential function of this subunit is neuronal. The photoreceptor phenotype of d alpha2delta-3 mutants resembles that of the calcium channel alpha1 mutant cacophony (cac), suggesting shared functions. We have examined in detail genotypes that survive to the third-instar stage. Electrophysiological recordings demonstrate that synaptic transmission is severely impaired in these mutants. Thus the alpha2delta calcium channel subunit is critical for calcium-dependent synaptic function. As such, this Drosophila isoform is the likely partner to the presynaptic calcium channel alpha1 subunit encoded by the cac locus. Consistent with this hypothesis, cacGFP fluorescence at the neuromuscular junction is reduced in d alpha2delta-3 mutants. This is the first characterization of an alpha2delta-3 mutant in any organism and indicates a necessary role for alpha2delta-3 in presynaptic vesicle release and calcium channel expression at active zones.

Indexed as

AnimalsAnimals, Genetically ModifiedCalciumCalcium ChannelsDrosophilaDrosophila ProteinsElectroretinographyEmbryo, NonmammalianGreen Fluorescent ProteinsMutationNeuromuscular JunctionPresynaptic TerminalsProtein SubunitsSynaptic TransmissionCalciumCalcium ChannelsDrosophila ProteinsGreen Fluorescent ProteinsProtein Subunits

Identifiers

PMID18171920
PMCPMC6671140

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.