Evidence map›Paper›PMID 21939738›Full record

ReviewNeuroscience2011

Dopamine release in the basal ganglia.

M E Rice, J C Patel, S J Cragg

Abstract readReview
In one paragraph

Review in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed
8.0field-weighted citation impact, top 1% 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

166 citing papers in PubMed, 282 citations in OpenAlex.

  1. Trial
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  11. Local Regulation of Striatal Dopamine Release Shifts from Predominantly Cholinergic in Mice to GABAergic in Macaques.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  13. Review
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  20. Review

106 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 2 institutions in 2 countries.

M E RiceDepartment of Neurosurgery, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. margaret.rice@nyu.edu
J C Patel
S J Cragg
New York University · USUniversity of Oxford · GB

Funding

Electrochemical Analysis of Dopamine ReleaseR01NS036362 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RICE, MARGARET E · 1997 to 2011
$3.3M
Electrochemical Analysis of Dopamine ReleaseR56NS036362 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RICE, MARGARET E · 2007 to 2007
$423k
Medical Research Council G0700932NINDS NIH HHS NS036362NINDS NIH HHS R01 NS036362NINDS NIH HHS R56 NS036362Parkinson's UK G-0803Parkinson's UK G-0808Parkinson's UK G-1103Parkinson's UK H-1003Parkinson's UK J-0901
6 · The paper itself

Abstract

Dopamine (DA) is a key transmitter in the basal ganglia, yet DA transmission does not conform to several aspects of the classic synaptic doctrine. Axonal DA release occurs through vesicular exocytosis and is action potential- and Ca²⁺-dependent. However, in addition to axonal release, DA neurons in midbrain exhibit somatodendritic release by an incompletely understood, but apparently exocytotic, mechanism. Even in striatum, axonal release sites are controversial, with evidence for DA varicosities that lack postsynaptic specialization, and largely extrasynaptic DA receptors and transporters. Moreover, DA release is often assumed to reflect a global response to a population of activities in midbrain DA neurons, whether tonic or phasic, with precise timing and specificity of action governed by other basal ganglia circuits. This view has been reinforced by anatomical evidence showing dense axonal DA arbors throughout striatum, and a lattice network formed by DA axons and glutamatergic input from cortex and thalamus. Nonetheless, localized DA transients are seen in vivo using voltammetric methods with high spatial and temporal resolution. Mechanistic studies using similar methods in vitro have revealed local regulation of DA release by other transmitters and modulators, as well as by proteins known to be disrupted in Parkinson's disease and other movement disorders. Notably, the actions of most other striatal transmitters on DA release also do not conform to the synaptic doctrine, with the absence of direct synaptic contacts for glutamate, GABA, and acetylcholine (ACh) on striatal DA axons. Overall, the findings reviewed here indicate that DA signaling in the basal ganglia is sculpted by cooperation between the timing and pattern of DA input and those of local regulatory factors.

Indexed as

AnimalsBasal GangliaBiological TransportDopamineDopaminergic NeuronsExocytosisModels, NeurologicalNeurotransmitter AgentsReceptors, DopamineSynaptic TransmissionDopamineNeurotransmitter AgentsReceptors, Dopamine

Identifiers

PMID21939738
PMCPMC3357127
OpenAlexW1989486566

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.