Evidence map›Paper›PMID 12514211›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Two intracellular pathways mediate metabotropic glutamate receptor-induced Ca2+ mobilization in dopamine neurons.

Hitoshi Morikawa, Kamran Khodakhah, John T Williams

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 155 citations in OpenAlex.

  1. The role of calcium stores in long-term potentiation and synaptic tagging and capture in mouse hippocampus.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  2. Endolysosomal TPCs regulate social behavior by controlling oxytocin secretion.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Article
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  7. Article
  8. Article
  9. Review
  10. Enhanced Sensitivity to Hyperpolarizing Inhibition in Mesoaccumbal Relative to Nigrostriatal Dopamine Neuron Subpopulations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  11. Article
  12. Article
  13. Dendritic Release of Neurotransmitters.Comprehensive Physiology · 2016
    Review
  14. Article
  15. Ryanodine-sensitive intracellular CaThe European journal of neuroscience · 2016
    Article
  16. Article
  17. Article
  18. Article
  19. Behavioral and Physiological Effects of a Novel Kappa-Opioid Receptor-Based DREADD in Rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Hitoshi MorikawaVollum Institute, Oregon Health and Science University, Portland, Oregon 97201, USA.
Kamran Khodakhah
John T Williams
Albert Einstein College of Medicine · USOregon Health & Science University · USVollum Institute · US

Funding

COCAINE: EFFECTS ON SINGLE NEURONSR01DA004523 · NIDA · OREGON HEALTH & SCIENCE UNIVERSITY · PI WILLIAMS, JOHN T · 1987 to 2025
$7.6M
Calcium Signaling in the Reward Circuit &Drug AddictionR01DA015687 · NIDA · UNIVERSITY OF TEXAS AUSTIN · PI MORIKAWA, HITOSHI · 2003 to 2013
$2.4M
NIDA NIH HHS DA04523NIDA NIH HHS R01 DA004523NIDA NIH HHS R01 DA015687
6 · The paper itself

Abstract

Activation of metabotropic glutamate receptors (mGluRs) causes membrane hyperpolarization in midbrain dopamine neurons. This hyperpolarization results from the opening of Ca(2+)-sensitive K(+) channels, which is mediated by the release of Ca(2+) from intracellular stores. Neurotransmitter-induced mobilization of Ca(2+) is generally ascribed to the action of inositol 1,4,5-triphosphate (IP(3)) in neurons. Here we show that the mGluR-mediated Ca(2+) mobilization in dopamine neurons is caused by two intracellular second messengers: IP(3) and cyclic ADP-ribose (cADPR). Focal activation of mGluRs, attained by synaptic release of glutamate or iontophoretic application of aspartate, induced a wave of Ca(2+) that spread over a distance of approximately 50 microm through dendrites and the soma. Simultaneous inhibition of both IP(3)- and cADPR-dependent pathways with heparin and 8-NH(2)-cADPR was required to block the mGluR-induced Ca(2+) release, indicating a redundancy in the signaling mechanism. Activation of ryanodine receptors was suggested to mediate the cADPR-dependent pathway, because ruthenium red, an antagonist of ryanodine receptors, inhibited the mGluR response only when the cADPR-dependent pathway was isolated by blocking the IP(3)-dependent pathway with heparin. Finally, the mGluR-mediated hyperpolarization was shown to induce a transient pause in the spontaneous firing of dopamine neurons. These results demonstrate that an excitatory neurotransmitter glutamate uses multiple intracellular pathways to exert an inhibitory control on the excitability of dopamine neurons.

Indexed as

Calcium SignalingSecond Messenger SystemsAnimalsCells, CulturedCyclic ADP-RiboseDopamineElectric ConductivityEvoked PotentialsInositol 1,4,5-TrisphosphateKineticsMesencephalonMicroscopy, ConfocalNeuronsPatch-Clamp TechniquesRatsRats, WistarCyclic ADP-RiboseDopamineInositol 1,4,5-TrisphosphateReceptors, Metabotropic GlutamateRyanodine Receptor Calcium Release Channel

Identifiers

PMID12514211
PMCPMC1408315
OpenAlexW2096118295

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.