Evidence map›Paper›PMID 21288471›Full record

ArticleNeuropharmacology2011

Concurrent upregulation of postsynaptic L-type Ca(2+) channel function and protein kinase A signaling is required for the periadolescent facilitation of Ca(2+) plateau potentials and dopamine D1 receptor modulation in the prefrontal cortex.

Li-Jun Heng, Julie A Markham, Xiu-Ti Hu, Kuei Y Tseng

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Illness Phase as a Key Assessment and Intervention Window for Psychosis.Biological psychiatry global open science · 2023
    Review
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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 3 institutions in 1 country.

Li-Jun HengDepartment of Cellular and Molecular Pharmacology, Rosalind Franklin University of Medicine and Science, The Chicago Medical School, 3333 Green Bay Rd., North Chicago, IL 60064, USA.
Julie A Markham
Xiu-Ti Hu
Kuei Y Tseng
Rosalind Franklin University of Medicine and Science · USRush University Medical Center · USUniversity of Maryland, Baltimore · US

Funding

Maryland's Organized Research Effort in Women's Health (MORE-WH)K12HD043489 · NICHD · UNIVERSITY OF MARYLAND BALTIMORE · PI TRACY, J. KATHLEEN · 2002 to 2016
$7.0M
Monoaminergic regulation of prefrontal cortex inhibition during adolescenceR01MH086507 · NIMH · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Kuei-Yuan Tseng · 2010 to 2026
$5.7M
COCAINE &MESOLIMBIC DOPAMINE ELECTROPHYSIOLOGYR01DA004093 · NIDA · WAYNE STATE UNIVERSITY · PI TSENG, KUEI-YUAN · 1986 to 2006
$547k
NICHD NIH HHS K12 HD043489NICHD NIH HHS K12HD043489-08NIDA NIH HHS R01 DA004093NIMH NIH HHS R01 MH086507
6 · The paper itself

Abstract

Further understanding of how prefrontal cortex (PFC) circuit change during postnatal development is of great interest due to its role in working memory and decision-making, two cognitive abilities that are refined late in adolescence and become altered in schizophrenia. While it is evident that dopamine facilitation of glutamate responses occurs during adolescence in the PFC, little is known about the cellular mechanisms that support these changes. Among them, a developmental facilitation of postsynaptic Ca(2+) function is of particular interest given its role in coordinating neuronal ensembles, a process thought to contribute to maturation of PFC function. Here we conducted whole-cell patch clamp recordings of deep-layer pyramidal neurons in PFC brain slices and determined how somatic-evoked Ca(2+)-mediated plateau depolarizations change throughout postnatal day (PD) 25 (juvenile) to adulthood (PD 80). Postsynaptic Ca(2+) potentials in the PFC increase in duration throughout postnatal development. A remarkable shift from short to prolonged depolarizations was observed after PD 40. This change is reflected by an enhancement of L-type Ca(2+) channel function and postsynaptic PKA signaling. We speculate that such a protracted developmental facilitation of Ca(2+) response in the PFC may contribute to improvement of working memory performance through adolescence.

Indexed as

AnimalsCalciumCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesExcitatory Postsynaptic PotentialsIn Vitro TechniquesMalePatch-Clamp TechniquesPrefrontal CortexPyramidal CellsRatsReceptors, Dopamine D1Signal TransductionUp-RegulationCalciumCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesReceptors, Dopamine D1

Identifiers

PMID21288471
PMCPMC3077898
OpenAlexW1982471973

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.