Evidence map›Paper›PMID 24599471›Full record

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

μ-Opioid inhibition of Ca2+ currents and secretion in isolated terminals of the neurohypophysis occurs via ryanodine-sensitive Ca2+ stores.

Cristina Velázquez-Marrero, Sonia Ortiz-Miranda, Héctor G Marrero, Edward E Custer, Steven N Treistman, José R Lemos

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Rational Design Biased Compounds against μ‑Opioid Receptor.ACS pharmacology & translational science · 2025
    Article
  2. Review
  3. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  4. Article
  5. Fentanyl Induces Rapid Onset Hyperalgesic Priming: Type I at Peripheral and Type II at Central Nociceptor Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  6. Article
  7. Neuronal NCX1 overexpression induces stroke resistance while knockout induces vulnerability via Akt.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016
    Article
  8. Article
  9. Article
  10. 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

6 authors at 1 institution in 1 country.

Cristina Velázquez-MarreroDepartment of Microbiology and Physiological Systems and Program in Neuroscience, University of Massachusetts Medical School, Worcester, Massachusetts 01605.
Sonia Ortiz-Miranda
Héctor G Marrero
Edward E Custer
Steven N Treistman
José R Lemos
University of Massachusetts Chan Medical School · US

Funding

The Role of Sensory Input to Mammalian Locomotion After the Loss of supraspinal.P20GM103642 · NIGMS · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI LASALDE-DOMINICCI, JOSE ANTONIO · 2013 to 2023
$20.6M
DEPOLARIZATION/SECRETION COUPLING IN NERVE TERMINALSR01NS029470 · NINDS · WORCESTER FOUNDATION FOR BIOMEDICAL RES · PI LEMOS, JOSE R · 1991 to 2012
$4.3M
ALCOHOL ACTION ON NERVE TERMINALS IN SELECTED STRAINSR01AA008003 · NIAAA · WORCESTER FOUNDATION FOR BIOMEDICAL RES · PI TREISTMAN, STEVEN N · 1989 to 2009
$3.5M
miRNA Regulation of Gene Expression in Alcohol Tolerance and WithdrawalR01AA017920 · NIAAA · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI PIETRZYKOWSKI, ANDRZEJ ZBIGNIEW, TREISTMAN, STEVEN N · 2009 to 2013
$2.0M
The Role of BK Channel Composition in Alcohol Tolerance and ConsumptionR01AA018038 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI TREISTMAN, STEVEN N · 2008 to 2012
$1.9M
MECHANISMS OF OPIOID ACTION ON PEPTIDE RELEASER01DA010487 · NIDA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LEMOS, JOSE R · 1998 to 2002
$866k
Peptide Release Regulated by Ca2+ from Neurosecretory GranulesR21NS063192 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LEMOS, JOSE R · 2009 to 2010
$393k
NIAAA NIH HHS R01 AA008003NIAAA NIH HHS R01 AA017920NIAAA NIH HHS R01 AA018038NIDA NIH HHS R01 DA010487NIDA NIH HHS R01DA10487NIGMS NIH HHS P20 GM103642NINDS NIH HHS R01 NS029470NINDS NIH HHS R01 NS29470NINDS NIH HHS R21 NS063192
6 · The paper itself

Abstract

μ-Opioid agonists have no effect on calcium currents (I(Ca)) in neurohypophysial terminals when recorded using the classic whole-cell patch-clamp configuration. However, μ-opioid receptor (MOR)-mediated inhibition of I(Ca) is reliably demonstrated using the perforated-patch configuration. This suggests that the MOR-signaling pathway is sensitive to intraterminal dialysis and is therefore mediated by a readily diffusible second messenger. Using the perforated patch-clamp technique and ratio-calcium-imaging methods, we describe a diffusible second messenger pathway stimulated by the MOR that inhibits voltage-gated calcium channels in isolated terminals from the rat neurohypophysis (NH). Our results show a rise in basal intracellular calcium ([Ca(2+)]i) in response to application of [D-Ala(2)-N-Me-Phe(4),Gly5-ol]-Enkephalin (DAMGO), a MOR agonist, that is blocked by D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP), a MOR antagonist. Buffering DAMGO-induced changes in [Ca(2+)]i with BAPTA-AM completely blocked the inhibition of both I(Ca) and high-K(+)-induced rises in [Ca(2+)]i due to MOR activation, but had no effect on κ-opioid receptor (KOR)-mediated inhibition. Given the presence of ryanodine-sensitive stores in isolated terminals, we tested 8-bromo-cyclic adenosine diphosphate ribose (8Br-cADPr), a competitive inhibitor of cyclic ADP-ribose (cADPr) signaling that partially relieves DAMGO inhibition of I(Ca) and completely relieves MOR-mediated inhibition of high-K(+)-induced and DAMGO-induced rises in [Ca(2+)]i. Furthermore, antagonist concentrations of ryanodine completely blocked MOR-induced increases in [Ca(2+)]i and inhibition of I(Ca) and high-K(+)-induced rises in [Ca(2+)]i while not affecting KOR-mediated inhibition. Antagonist concentrations of ryanodine also blocked MOR-mediated inhibition of electrically-evoked increases in capacitance. These results strongly suggest that a key diffusible second messenger mediating the MOR-signaling pathway in NH terminals is [Ca(2+)]i released by cADPr from ryanodine-sensitive stores.

Indexed as

Analgesics, OpioidAnimalsCalciumEnkephalin, Ala(2)-MePhe(4)-Gly(5)-MalePituitary Gland, PosteriorPresynaptic TerminalsRatsRats, Sprague-DawleyReceptors, Opioid, muRyanodineAnalgesics, OpioidCalciumEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Receptors, Opioid, muRyanodineexocytosisICaMOR modulationNH terminalsRyR

Identifiers

PMID24599471
PMCPMC3942588
OpenAlexW2092963556

What Socratic 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 Socratic graph.