Evidence map›Paper›PMID 29434376›Full record

ReviewNature neuroscience2018

Memory formation depends on both synapse-specific modifications of synaptic strength and cell-specific increases in excitability.

John Lisman, Katherine Cooper, Megha Sehgal, Alcino J Silva

Abstract readReview
In one paragraph

Review in Nature neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 1 pooled it
–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

175 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  16. Long Term High-Salt Diet Induces Cognitive Impairments via Down-Regulating SHANK1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  17. Article
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115 more citing papers are in PubMed but not listed here.

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.

John LismanDepartment of Biology, Brandeis University, Waltham, MA, USA.
Katherine CooperDepartment of Biology, Brandeis University, Waltham, MA, USA.
Megha SehgalDepartment of Neurobiology, Department of Psychology, Department of Psychiatry and Biobehavioral Sciences, Integrative Center for Learning and Memory, and Brain Research Institute, University of California, Los Angeles, Los Angeles, CA, USA.
Alcino J SilvaDepartment of Biology, Brandeis University, Waltham, MA, USA. alcinojsilva@att.net.

Funding

Towards a Complete Description of the Circuitry Underlying Sharp Wave-Mediated Memory ReplayU19NS104590 · NINDS · STANFORD UNIVERSITY · PI SCHNITZER, MARK J · 2017 to 2021
$13.2M
Molecular, Cellular and Circuit Mechanisms for Age-Related Deficits in Memory-LinkingRF1AG013622 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SILVA, ALCINO J. · 2017 to 2022
$4.9M
CCR5 Activation and Cognitive Dysfunction Caused by HIV-ProteinsR01NS106969 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SILVA, ALCINO J. · 2017 to 2021
$3.7M
Molecular, Cellular and Circuit Mechnisms for Memory-linking deficits in Psychiatric DisordersR01MH113071 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SILVA, ALCINO J. · 2017 to 2021
$2.3M
Towards a Complete Description of the Circuitry Underlying Memory replay.U01NS090583 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI SOLTESZ, IVAN · 2014 to 2016
$2.1M
Role of CaMKII in memory storageR01NS103168 · NINDS · BRANDEIS UNIVERSITY · PI GRIFFITH, LESLIE C · 2017 to 2021
$1.8M
CRCNS: Neural signals that maintain/refresh LTP and memoryR01DA043195 · NIDA · BRANDEIS UNIVERSITY · PI GRIFFITH, LESLIE C · 2017 to 2019
$1.1M
Role of CaMKII in memory storageR56NS096710 · NINDS · BRANDEIS UNIVERSITY · PI GRIFFITH, LESLIE C · 2016 to 2016
$484k
NIA NIH HHS RF1 AG013622NIDA NIH HHS R01 DA043195NIMH NIH HHS R01 MH113071NINDS NIH HHS R01 NS103168NINDS NIH HHS R01 NS106969NINDS NIH HHS R56 NS096710NINDS NIH HHS U01 NS090583NINDS NIH HHS U19 NS104590
6 · The paper itself

Abstract

The modification of synaptic strength produced by long-term potentiation (LTP) is widely thought to underlie memory storage. Indeed, given that hippocampal pyramidal neurons have >10,000 independently modifiable synapses, the potential for information storage by synaptic modification is enormous. However, recent work suggests that CREB-mediated global changes in neuronal excitability also play a critical role in memory formation. Because these global changes have a modest capacity for information storage compared with that of synaptic plasticity, their importance for memory function has been unclear. Here we review the newly emerging evidence for CREB-dependent control of excitability and discuss two possible mechanisms. First, the CREB-dependent transient change in neuronal excitability performs a memory-allocation function ensuring that memory is stored in ways that facilitate effective linking of events with temporal proximity (hours). Second, these changes may promote cell-assembly formation during the memory-consolidation phase. It has been unclear whether such global excitability changes and local synaptic mechanisms are complementary. Here we argue that the two mechanisms can work together to promote useful memory function.

Indexed as

AnimalsCyclic AMP Response Element-Binding ProteinHumansLong-Term PotentiationMemoryNeuronal PlasticityNeuronsSynapsesCREB1 protein, humanCyclic AMP Response Element-Binding Protein

Identifiers

PMID29434376
PMCPMC5915620

What OpenQuestion holds

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Read underepoch 390

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.