Evidence map›Paper›PMID 25966692›Full record

ReviewCurrent molecular pharmacology2015

Cav1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells.

David H F Vandael, Andrea Marcantoni, Emilio Carbone

Abstract readReview
In one paragraph

Review in Current molecular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. The Leucine-Rich Repeat Kinase 2 Variant LRRK2International journal of molecular sciences · 2025
    Article
  2. Article
  3. Review
  4. CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 2023
    Review
  5. Snapin Specifically Up-Regulates CaInternational journal of molecular sciences · 2021
    Article
  6. Article
  7. Article
  8. De novo CACNA1D CaPflugers Archiv : European journal of physiology · 2020
    Review
  9. Diurnal properties of voltage-gated CaThe Journal of physiology · 2020
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Old and emerging concepts on adrenal chromaffin cell stimulus-secretion coupling.Pflugers Archiv : European journal of physiology · 2018
    Article
  15. Roles of NaPflugers Archiv : European journal of physiology · 2018
    Review
  16. L-type calcium channels in exocytosis and endocytosis of chromaffin cells.Pflugers Archiv : European journal of physiology · 2018
    Review
  17. GABAPflugers Archiv : European journal of physiology · 2018
    Review
  18. Activity-Dependent Facilitation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  19. Article
  20. Regulation of L-type CaCell calcium · 2017
    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.

David H F Vandael
Andrea Marcantoni
Emilio CarboneDepartment of Drug Science, Corso Raffaello 30, I - 10125 Torino, Italy. emilio.carbone@unito.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal and neuroendocrine L-type calcium channels (Cav1.2, Cav1.3) open readily at relatively low membrane potentials and allow Ca(2+) to enter the cells near resting potentials. In this way, Cav1.2 and Cav1.3 shape the action potential waveform, contribute to gene expression, synaptic plasticity, neuronal differentiation, hormone secretion and pacemaker activity. In the chromaffin cells (CCs) of the adrenal medulla, Cav1.3 is highly expressed and is shown to support most of the pacemaking current that sustains action potential (AP) firings and part of the catecholamine secretion. Cav1.3 forms Ca(2+)-nanodomains with the fast inactivating BK channels and drives the resting SK currents. These latter set the inter-spike interval duration between consecutive spikes during spontaneous firing and the rate of spike adaptation during sustained depolarizations. Cav1.3 plays also a primary role in the switch from "tonic" to "burst" firing that occurs in mouse CCs when either the availability of voltage-gated Na channels (Nav) is reduced or the β2 subunit featuring the fast inactivating BK channels is deleted. Here, we discuss the functional role of these "neuron-like" firing modes in CCs and how Cav1.3 contributes to them. The open issue is to understand how these novel firing patterns are adapted to regulate the quantity of circulating catecholamines during resting condition or in response to acute and chronic stress.

Indexed as

Action PotentialsAnimalsCalcium Channels, L-TypeCatecholaminesChromaffin CellsHumansMiceNeuronsSodium Channel BlockersTetrodotoxinCACNA1D protein, humanCalcium Channels, L-TypeCatecholaminesSodium Channel BlockersTetrodotoxin

Identifiers

PMID25966692
PMCPMC5384372

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.