Evidence map›Paper›PMID 23390312›Full record

ArticleJournal of neurophysiology2013

A role for TREK1 in generating the slow afterhyperpolarization in developing starburst amacrine cells.

Kevin J Ford, David A Arroyo, Jeremy N Kay, Eric E Lloyd, Robert M Bryan, Joshua R Sanes, Marla B Feller

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. The Variety of Mechanosensitive Ion Channels in Retinal Neurons.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Retinal Axon Interplay for Binocular Mapping.Frontiers in neural circuits · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Spontaneous Network Activity and Synaptic Development.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014
    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

7 authors at 3 institutions in 1 country.

Kevin J FordDepartment of Molecular and Cellular Biology, University of California, Berkeley, CA, USA.
David A Arroyo
Jeremy N Kay
Eric E Lloyd
Robert M Bryan
Joshua R Sanes
Marla B Feller
Harvard University · USBaylor College of Medicine · USUniversity of California, Berkeley · US

Funding

The Function of Neural Activity in Developing RetinaR01EY013528 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Marla Feller · 2002 to 2026
$8.1M
EDHF in the Cerebral CirculationR01NS046666 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI BRYAN, ROBERT M · 2005 to 2009
$1.7M
Function of Two-Pore Domain K Channels in Vascular Smooth MuscleR21HL098921 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI BRYAN, ROBERT M · 2010 to 2011
$422k
NEURAL INTERACTIONS IN THE VERTEBRATE RETINAR01EY002207 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI OYSTER, CLYDE W. · 1985 to 1988
–
NEI NIH HHS R01 EY013528NEI NIH HHS R01-EY-013528NEI NIH HHS R01-EY-022073R01NHLBI NIH HHS R21-HL-098921NINDS NIH HHS F31-NS-614663NINDS NIH HHS NS-046666
6 · The paper itself

Abstract

Slow afterhyperpolarizations (sAHPs) play an important role in establishing the firing pattern of neurons that in turn influence network activity. sAHPs are mediated by calcium-activated potassium channels. However, the molecular identity of these channels and the mechanism linking calcium entry to their activation are still unknown. Here we present several lines of evidence suggesting that the sAHPs in developing starburst amacrine cells (SACs) are mediated by two-pore potassium channels. First, we use whole cell and perforated patch voltage clamp recordings to characterize the sAHP conductance under different pharmacological conditions. We find that this conductance was calcium dependent, reversed at EK, blocked by barium, insensitive to apamin and TEA, and activated by arachidonic acid. In addition, pharmacological inhibition of calcium-activated phosphodiesterase reduced the sAHP. Second, we performed gene profiling on isolated SACs and found that they showed strong preferential expression of the two-pore channel gene kcnk2 that encodes TREK1. Third, we demonstrated that TREK1 knockout animals exhibited an altered frequency of retinal waves, a frequency that is set by the sAHPs in SACs. With these results, we propose a model in which depolarization-induced decreases in cAMP lead to disinhibition of the two-pore potassium channels and in which the kinetics of this biochemical pathway dictate the slow activation and deactivation of the sAHP conductance. Our model offers a novel pathway for the activation of a conductance that is physiologically important.

Indexed as

Membrane PotentialsAction PotentialsAmacrine CellsAnimalsArachidonic AcidCalciumMiceMice, Inbred C57BLMice, KnockoutPotassium Channel BlockersPotassium Channels, Tandem Pore DomainTranscription, GeneticArachidonic AcidCalciumPotassium Channel Blockerspotassium channel protein TREK-1Potassium Channels, Tandem Pore Domaincalcium imaginggene profilingmultielectrode array recordingperforated patchretinaretinal waves

Identifiers

PMID23390312
PMCPMC3652223
OpenAlexW2009340149

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.