Evidence map›Paper›PMID 24795571›Full record

ArticleFrontiers in neural circuits2014

Dopamine-enabled anti-Hebbian timing-dependent plasticity in prefrontal circuitry.

Hongyu Ruan, Taixiang Saur, Wei-Dong Yao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neural circuits, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Adaptive control of synaptic plasticity integrates micro- and macroscopic network function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
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  10. Achieving stable dynamics in neural circuits.PLoS computational biology · 2020
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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

3 authors at 1 institution in 1 country.

Hongyu RuanHarvard Medical School - New England Primate Research Center Southborough, MA, USA ; Department of Psychiatry, Beth Israel Deaconess Medical Center Boston, MA, USA.
Taixiang SaurHarvard Medical School - New England Primate Research Center Southborough, MA, USA ; Department of Psychiatry, Beth Israel Deaconess Medical Center Boston, MA, USA.
Wei-Dong YaoHarvard Medical School - New England Primate Research Center Southborough, MA, USA ; Department of Psychiatry, Beth Israel Deaconess Medical Center Boston, MA, USA.
Harvard University · US

Funding

New England Primate Research Center Base GrantP51OD011103 · OD · HARVARD MEDICAL SCHOOL · PI FLIER, JEFFREY S · 2012 to 2013
$24.7M
Dopaminergic Enabling of Synaptic Plasticity in Prefrontal CircuitsR01DA032283 · NIDA · UPSTATE MEDICAL UNIVERSITY · PI YAO, WEI-DONG · 2011 to 2015
$1.7M
NIDA NIH HHS DA032283NIDA NIH HHS R01 DA032283NIH HHS OD011103NIH HHS P51 OD011103
6 · The paper itself

Abstract

Spike timing-dependent plasticity (STDP) of glutamatergic synapses is a Hebbian associative plasticity that may underlie certain forms of learning. A cardinal feature of STDP is its dependence on the temporal order of presynaptic and postsynaptic spikes during induction: pre-post (positive) pairings induce t-LTP (timing-dependent long-term potentiation) whereas post-pre (negative) pairings induce t-LTD (timing-dependent long-term depression). Dopamine (DA), a reward signal for behavioral learning, is believed to exert powerful modulations on synapse strength and plasticity, but its influence on STDP has remained incompletely understood. We previously showed that DA extends the temporal window of t-LTP in the prefrontal cortex (PFC) from +10 to +30 ms, gating Hebbian t-LTP. Here, we examined DA modulation of synaptic plasticity induced at negative timings in layer V pyramidal neurons on mouse medial PFC slices. Using a negative timing STDP protocol (60 post-pre pairings at 0.1 Hz, δt = -30 ms), we found that DA applied during post-pre pairings did not produce LTD, but instead enabled robust LTP. This anti-Hebbian t-LTP depended on GluN2B-containing NMDA receptors. Blocking D1- (D1Rs), but not D2- (D2Rs) class DA receptors or disrupting cAMP/PKA signaling in pyramidal neurons also abolished this atypical t-LTP, indicating that it was mediated by postsynaptic D1R-cAMP/PKA signaling in excitatory synapses. Unlike DA-enabled Hebbian t-LTP that requires suppression of GABAergic inhibition and cooperative actions of both D1Rs and D2Rs in separate PFC excitatory and inhibitory circuits, DA-enabled anti-Hebbian t-LTP occurred under intact inhibitory transmission and only required D1R activation in excitatory circuit. Our results establish DA as a potent modulator of coincidence detection during associative synaptic plasticity and suggest a mechanism by which DA facilitates input-target association during reward learning and top-down information processing in PFC circuits.

Indexed as

AnimalsDopamineDopamine AgonistsDopamine AntagonistsLong-Term PotentiationMaleMiceNeuronsPrefrontal CortexReceptors, Dopamine D1Receptors, Dopamine D2Receptors, N-Methyl-D-AspartateDopamineDopamine AgonistsDopamine AntagonistsNR2B NMDA receptorReceptors, Dopamine D1Receptors, Dopamine D2Receptors, N-Methyl-D-AspartatedopamineglutamateHebbianlearningrewardSTDP

Identifiers

PMID24795571
PMCPMC4005942
OpenAlexW2136341141

What OpenQuestion holds

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LicenceCC BY
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.