Evidence map›Paper›PMID 9254669›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

Kappa-opioid receptor activation modulates Ca2+ currents and secretion in isolated neuroendocrine nerve terminals.

K I Rusin, D R Giovannucci, E L Stuenkel, H C Moises

Open access · bronzeAbstract read
PubMed Full text at PMC
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

46 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. Kappa opioid receptor control of motivated behavior revisited.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Recommended Opioid Receptor Tool Compounds: ComparativeACS pharmacology & translational science · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. The Kappa Opioid Receptor System in Temporal Lobe Epilepsy.Handbook of experimental pharmacology · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Strategies for DevelopingThe Journal of pharmacology and experimental therapeutics · 2020
    Review
  17. Cocaine Dysregulates Dynorphin Modulation of Inhibitory Neurotransmission in the Ventral Pallidum in a Cell-Type-Specific Manner.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

K I RusinDepartment of Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0622, USA.
D R Giovannucci
E L Stuenkel
H C Moises
University of Michigan–Ann Arbor · US

Funding

OPIOID AND G-PROTEIN REGULATION OF CALCIUM CURRENTSR01DA003365 · NIDA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOISES, HYLAN C · 1986 to 2001
$421k
NIDA NIH HHS DA03365
6 · The paper itself

Abstract

Whole-cell patch-clamp recordings were performed together with time-resolved measurements of membrane capacitance (Cm) in nerve terminals acutely dissociated from neurohypophysis of adult rats to investigate modulation of Ca2+ currents and secretion by activation of opioid receptors. Bath superfusion of the kappa-opioid agonists U69,593 (0.3-1 microM), dynorphin A (1 microM), or U50,488H (1-3 microM) reversibly suppressed the peak amplitude of Ca2+ currents 32. 7 +/- 2.7% (in 41 of 56 terminals), 37.4 +/- 5.3% (in 5 of 8 terminals), and 33.5 +/- 8.1% (in 5 of 10 terminals), respectively. In contrast, tests in 11 terminals revealed no effect of the mu-opioid agonist [D-Pen2,5]-enkephalin (1-3 microM; n = 7) or of the delta-agonist Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol (1 microM; n = 4) on Ca2+ currents. Three components of high-threshold current were distinguished on the basis of their sensitivity to blockade by omega-conotoxin GVIA, nicardipine, and omega-conotoxin MVIIC: N-, L-, and P/Q-type current, respectively. Administration of U69,593 inhibited N-type current in these nerve terminals on average 32%, whereas L-type current was reduced 64%, and P/Q-type current was inhibited 28%. Monitoring of changes in Cm in response to brief depolarizing steps revealed that the kappa-opioid-induced reductions in N-, L-, or P/Q-type currents were accompanied by attenuations in two kinetically distinct components of Ca2+-dependent exocytotic release. These data provide strong evidence of a functional linkage between blockade of Ca2+ influx through voltage-dependent Ca2+ channels and inhibitory modulation of release by presynaptic opioid receptors in mammalian central nerve endings.

Indexed as

AnimalsCalciumDifferential ThresholdElectric ConductivityExocytosisIn Vitro TechniquesMaleNarcoticsNerve EndingsNeurosecretory SystemsRatsReceptors, Opioid, kappaCalciumNarcoticsReceptors, Opioid, kappa

Identifiers

PMID9254669
PMCPMC6573146
OpenAlexW1898469558

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.