Evidence map›Paper›PMID 22553014›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

CNS dopamine transmission mediated by noradrenergic innervation.

Caroline C Smith, Robert W Greene

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

98 citing papers in PubMed, 177 citations in OpenAlex.

  1. Distinct Roles of Dopamine and Noradrenaline in Incidental Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Trial
  2. How Administration of the Beta-Blocker Propranolol Before Extinction can Prevent the Return of Fear.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Trial
  3. Article
  4. Article
  5. The hippocampus as a generative model.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  6. Stimulation of CaScience signaling · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Stimulus-Dependent Dopamine Dynamics from Locus Coeruleus Axons.bioRxiv : the preprint server for biology · 2025
    Article
  11. Functional and Regional Specificity of Noradrenergic Signaling for Encoding and Retrieval of Associative Recognition Memory in the Rat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  12. Article
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  15. Article
  16. Review
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  18. Article
  19. Review
  20. Review

38 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

2 authors at 2 institutions in 1 country.

Caroline C SmithDepartment of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Robert W Greene
Dallas VA Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Dopamine Modulation of NMDA Receptor Synaptic ResponsesR01MH080297 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI GREENE, ROBERT W · 2008 to 2012
$1.6M
NIMH NIH HHS 5R01MH080297NIMH NIH HHS R01 MH080297
6 · The paper itself

Abstract

The presynaptic source of dopamine in the CA1 field of dorsal hippocampus is uncertain due to an anatomical mismatch between dopaminergic terminals and receptors. We show, in an in vitro slice preparation from C57BL/6 male mice, that a dopamine (DA) D1 receptor (D1R)-mediated enhancement in glutamate synaptic transmission occurs following release of endogenous DA with amphetamine exposure. It is assumed DA is released from terminals innervating from the ventral tegmental area (VTA) even though DA transporter (DAT)-positive fibers are absent in hippocampus, a region with abundant D1Rs. It has been suggested this results from a lack of DAT expression on VTA terminals rather than a lack of these terminals per se. Neither a knockdown of tyrosine hydroxylase (TH) expression in the VTA by THsiRNA, delivered locally, by adeno-associated viral vector, nor localized pharmacological blockade of DAT to prevent amphetamine uptake into DA terminals, has any effect on the D1R synaptic, enhancement response to amphetamine. However, either a decrease in TH expression in the locus ceruleus (LC) or a blockade of the norepinephrine (NE) transporter prevents the DA-mediated response, indicating LC terminals can release both NE and DA. These findings suggest noradrenergic fibers may be the primary source of DA release in hippocampus and corresponding DA-mediated increase in synaptic transmission. Accordingly, these data imply the LC may have a role in DA transmission in the CNS in response to drugs of abuse, and potentially, under physiological conditions.

Indexed as

Adrenergic NeuronsAnimalsCells, CulturedDopamineHippocampusLocus CoeruleusMaleMiceMice, Inbred C57BLNeural PathwaysNeurotransmitter AgentsReceptors, DopamineSynaptic TransmissionDopamineNeurotransmitter AgentsReceptors, Dopamine

Identifiers

PMID22553014
PMCPMC3371362
OpenAlexW2027882681

What OpenQuestion holds

Textmetadata
LicenceTDM
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.