Evidence map›Paper›PMID 20011119›Full record

ArticlePLoS computational biology2009

Cortical gamma rhythms modulate NMDAR-mediated spike timing dependent plasticity in a biophysical model.

Shane Lee, Kamal Sen, Nancy Kopell

Abstract read
In one paragraph

Article in PLoS computational biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

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  15. GABAB receptor-mediated, layer-specific synaptic plasticity reorganizes gamma-frequency neocortical response to stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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.

Shane LeeProgram in Neuroscience, Boston University, Boston, Massachusetts, United States of America. shane@math.bu.edu
Kamal Sen
Nancy Kopell

Funding

TRAINING IN NEUROSCIENCET32MH020064 · NIMH · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI ELDRED, WILLIAM D · 2000 to 2009
$2.1M
Auditory Cortical Processing of Communication SoundsR01DC007610 · NIDCD · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI SEN, KAMAL K · 2006 to 2010
$1.9M
NIDCD NIH HHS 1 RO1 DC-007610 - 01A1NIDCD NIH HHS R01 DC007610NIMH NIH HHS T32 MH020064NIMH NIH HHS T32 MH020064-07NIMH NIH HHS T32 MH020064-08
6 · The paper itself

Abstract

Spike timing dependent plasticity (STDP) has been observed experimentally in vitro and is a widely studied neural algorithm for synaptic modification. While the functional role of STDP has been investigated extensively, the effect of rhythms on the precise timing of STDP has not been characterized as well. We use a simplified biophysical model of a cortical network that generates pyramidal interneuronal gamma rhythms (PING). Plasticity via STDP is investigated at the excitatory pyramidal cell synapse from a gamma frequency (30-90 Hz) input independent of the network gamma rhythm. The input may represent a corticocortical or an information-specific thalamocortical connection. This synapse is mediated by N-methyl-D-aspartate receptor mediated (NMDAR) currents. For distinct network and input frequencies, the model shows robust frequency regimes of potentiation and depression, providing a mechanism by which responses to certain inputs can potentiate while responses to other inputs depress. For potentiating regimes, the model suggests an optimal amount and duration of plasticity that can occur, which depends on the time course for the decay of the postsynaptic NMDAR current. Prolonging the duration of the input beyond this optimal time results in depression. Inserting pauses in the input can increase the total potentiation. The optimal pause length corresponds to the decay time of the NMDAR current. Thus, STDP in this model provides a mechanism for potentiation and depression depending on input frequency and suggests that the slow NMDAR current decay helps to regulate the optimal amplitude and duration of the plasticity. The optimal pause length is comparable to the time scale of the negative phase of a modulatory theta rhythm, which may pause gamma rhythm spiking. Our pause results may suggest a novel role for this theta rhythm in plasticity. Finally, we discuss our results in the context of auditory thalamocortical plasticity.

Indexed as

Models, NeurologicalNeuronal PlasticityAnimalsAuditory CortexElectroencephalographyGlutamineReceptors, N-Methyl-D-AspartateGlutamineReceptors, N-Methyl-D-Aspartate

Identifiers

PMID20011119
PMCPMC2782132

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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.