Evidence map›Paper›PMID 21689107›Full record

ArticleJournal of neurochemistry2011

Subsecond regulation of striatal dopamine release by pre-synaptic KATP channels.

Jyoti C Patel, Paul Witkovsky, William A Coetzee, Margaret E Rice

Abstract read
In one paragraph

Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 35% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Energy-dependent modulation of nucleus accumbens output via K-ATP channel activity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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.

Jyoti C PatelDepartment of Neurosurgery, New York University School of Medicine, New York, New York 10016, USA. jyotiben.patel@nyumc.org
Paul Witkovsky
William A Coetzee
Margaret E Rice
New York University · US

Funding

Electrochemical Analysis of Dopamine ReleaseR01NS036362 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RICE, MARGARET E · 1997 to 2011
$3.3M
Potassium Channels as Macromolecular ComplexesR01HL085820 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COETZEE, WILLIAM A, NEUBERT, THOMAS A · 2008 to 2013
$3.2M
Electrochemical Analysis of Dopamine ReleaseR56NS036362 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RICE, MARGARET E · 2007 to 2007
$423k
NHLBI NIH HHS HL085820NHLBI NIH HHS R01 HL085820NINDS NIH HHS NS036362NINDS NIH HHS R01 NS036362NINDS NIH HHS R56 NS036362
6 · The paper itself

Abstract

ATP-sensitive K(+) (K(ATP)) channels are composed of pore-forming subunits, typically Kir6.2 in neurons, and regulatory sulfonylurea receptor subunits. In dorsal striatum, activity-dependent H(2)O(2) produced from glutamate receptor activation inhibits dopamine release via K(ATP) channels. Sources of modulatory H(2)O(2) include striatal medium spiny neurons, but not dopaminergic axons. Using fast-scan cyclic voltammetry in guinea-pig striatal slices and immunohistochemistry, we determined the time window for H(2)O(2)/K(ATP)-channel-mediated inhibition and assessed whether modulatory K(ATP) channels are on dopaminergic axons. Comparison of paired-pulse suppression of dopamine release in the absence and presence of glibenclamide, a K(ATP)-channel blocker, or mercaptosuccinate, a glutathione peroxidase inhibitor that enhances endogenous H(2)O(2) levels, revealed a time window for inhibition of 500-1000 ms after stimulation. Immunohistochemistry demonstrated localization of Kir6.2 K(ATP)-channel subunits on dopaminergic axons. Consistent with the presence of functional K(ATP) channels on dopaminergic axons, K(ATP)-channel openers, diazoxide and cromakalim, suppressed single-pulse evoked dopamine release. Although cholinergic interneurons that tonically regulate dopamine release also express K(ATP) channels, diazoxide did not induce the enhanced frequency responsiveness of dopamine release seen with nicotinic-receptor blockade. Together, these studies reveal subsecond regulation of striatal dopamine release by endogenous H(2)O(2) acting at K(ATP) channels on dopaminergic axons, including a role in paired-pulse suppression.

Indexed as

Analysis of VarianceAnimalsATP-Binding Cassette TransportersBiophysicsCorpus StriatumDiazoxideDopamineDopamine AgonistsElectric StimulationElectrochemistryGlyburideGuinea PigsHydrogen PeroxideHypoglycemic AgentsIn Vitro TechniquesKATP Channels2-thiomalic acidATP-Binding Cassette TransportersDiazoxideDopamineDopamine AgonistsGlyburideHydrogen PeroxideHypoglycemic AgentsKATP ChannelsMecamylamineNicotinic AntagonistsPotassium Channels, Inwardly RectifyingQuinpiroleReceptors, DrugSulfonylurea ReceptorsThiomalatesTyrosine 3-MonooxygenaseuK-ATP-1 potassium channel

Identifiers

PMID21689107
PMCPMC3369699
OpenAlexW1599228558

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.