Evidence map›Paper›PMID 20554832›Full record

ArticleJournal of neurophysiology2010

The h current is a candidate mechanism for regulating the sliding modification threshold in a BCM-like synaptic learning rule.

Rishikesh Narayanan, Daniel Johnston

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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.

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3 · Its place in the literature

Who cites it

59 citing papers in PubMed.

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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

2 authors.

Rishikesh NarayananCenter for Learning and Memory, The University of Texas, Austin, Texas 78712-0805, USA.
Daniel Johnston

Funding

Regulation of Neuronal Excitability (P01)P01NS037444 · NINDS · UNIVERSITY OF TEXAS AUSTIN · PI JOHNSTON, DANIEL · 1999 to 2008
$8.4M
CELLULAR INFORMATION PROCESSING IN THE HIPPOCAMPUSR01MH048432 · NIMH · UNIVERSITY OF TEXAS AUSTIN · PI JOHNSTON, DANIEL · 1991 to 2012
$3.8M
PHARMACOLOGY OF MOSSY FIBER SYNAPTIC PLASTICITYR37MH044754 · NIMH · UNIVERSITY OF TEXAS AUSTIN · PI JOHNSTON, DANIEL · 1989 to 2008
$3.2M
NIMH NIH HHS MH-44754NIMH NIH HHS MH-48432NINDS NIH HHS NS-37444
6 · The paper itself

Abstract

Hebbian synaptic plasticity acts as a positive feedback mechanism and can destabilize a neuronal network unless concomitant homeostatic processes that counterbalance this instability are activated. Within a Bienenstock-Cooper-Munro (BCM)-like plasticity framework, such compensation is achieved through a modification threshold that slides in an activity-dependent fashion. Although the BCM-like plasticity framework has been a useful formulation to understand synaptic plasticity and metaplasticity, a mechanism for the activity-dependent regulation of this modification threshold has remained an open question. In this simulation study based on CA1 pyramidal cells, we use a modification of the calcium-dependent hypothesis proposed elsewhere and show that a change in the hyperpolarization-activated, nonspecific-cation h current is capable of shifting the modification threshold. Based on the direction of such a shift in relation to changes in the h current, and supported by previous experimental results, we argue that the h current fits the requirements for an activity-dependent regulator of this modification threshold. Additionally, using the same framework, we show that multiple voltage- and ligand-gated ion channels present in a neuronal compartment can regulate the modification threshold through complex interactions among themselves. Our results underscore the heavy mutual interdependence of synaptic and intrinsic properties/plasticity in regulating learning and homeostasis in single neurons and their networks under both physiological and pathological brain states.

Indexed as

AnimalsCalciumFeedback, PhysiologicalHippocampusIon ChannelsModels, NeurologicalNeuronal PlasticityPyramidal CellsReceptors, GlutamateSynapsesCalciumIon ChannelsReceptors, Glutamate

Identifiers

PMID20554832
PMCPMC2934916

What OpenQuestion holds

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Registered trials

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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.