Evidence map›Paper›PMID 23796633›Full record

ReviewNeurobiology of learning and memory2013

Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: implications for pain and memory.

Elizabeth J Rahn, Mikael C Guzman-Karlsson, J David Sweatt

Abstract readReview
In one paragraph

Review in Neurobiology of learning and memory, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing 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

58 citing papers in PubMed.

  1. Role of CPEBs in Learning and Memory.Journal of neurochemistry · 2025
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Blocking the Spinal Fbxo3/CARM1/KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
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.

Elizabeth J RahnDepartment of Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA.
Mikael C Guzman-Karlsson
J David Sweatt

Funding

Biochemical Mechanisms of Neural PlasticityR01MH057014 · NIMH · VANDERBILT UNIVERSITY · PI WINDER, DANNY G. · 1996 to 2019
$9.3M
UAB Research Training Program in Neurobiology of Cognition and Cognitive DisordersT32NS061788 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Farah Dominique Lubin · 2008 to 2026
$4.5M
Epigenetic Modifications of BDNF and trkB Genes Underlie Pain PlasticityR01NR012686 · NINR · UNIVERSITY OF MARYLAND BALTIMORE · PI DORSEY, SUSAN G, SWEATT, JOHN DAVID · 2010 to 2014
$3.2M
DNA Methylation in Memory FormationR01MH091122 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2011 to 2015
$1.8M
Trophic Interactions of Nerve and MuscleR01AG031722 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2007 to 2011
$1.6M
NIA NIH HHS R01 AG031722NIMH NIH HHS R01 MH057014NIMH NIH HHS R01 MH091122NINDS NIH HHS 3T32NS061788NINDS NIH HHS T32 NS061788NINR NIH HHS NR012686NINR NIH HHS R01 NR012686PHS HHS 031722PHS HHS 091122PHS HHS 57014
6 · The paper itself

Abstract

Sensitization is a form of non-associative conditioning in which amplification of behavioral responses can occur following presentation of an aversive or noxious stimulus. Understanding the cellular and molecular underpinnings of sensitization has been an overarching theme spanning the field of learning and memory as well as that of pain research. In this review we examine how sensitization, both in the context of learning as well as pain processing, shares evolutionarily conserved behavioral, cellular/synaptic, and epigenetic mechanisms across phyla. First, we characterize the behavioral phenomenon of sensitization both in invertebrates and vertebrates. Particular emphasis is placed on long-term sensitization (LTS) of withdrawal reflexes in Aplysia following aversive stimulation or injury, although additional invertebrate models are also covered. In the context of vertebrates, sensitization of mammalian hyperarousal in a model of post-traumatic stress disorder (PTSD), as well as mammalian models of inflammatory and neuropathic pain is characterized. Second, we investigate the cellular and synaptic mechanisms underlying these behaviors. We focus our discussion on serotonin-mediated long-term facilitation (LTF) and axotomy-mediated long-term hyperexcitability (LTH) in reduced Aplysia systems, as well as mammalian spinal plasticity mechanisms of central sensitization. Third, we explore recent evidence implicating epigenetic mechanisms in learning- and pain-related sensitization. This review illustrates the fundamental and functional overlay of the learning and memory field with the pain field which argues for homologous persistent plasticity mechanisms in response to sensitizing stimuli or injury across phyla.

Indexed as

Epigenesis, GeneticAnimalsAplysiaCentral Nervous System SensitizationConditioning, PsychologicalHumansMemoryMiceNeuronal PlasticityPainRatsSignal Transduction4EBP5-aza5-azacytidine5-HTAplysiaBDNFbrain derived neurotrophic factorCa(2+)calciumcalmodulin-dependent protein kinase IICAMKIIcAMPcAMP-dependent protein kinasecAMP response elementcAMP response element binding proteinCBSCCAAT enhancer binding proteinCCIC/EBPCentral sensitizationCFAcGMPchronic constriction injurycomplete Freund’s adjuvantCOX-2CPBCPEBCRECREBCREB-binding proteincyclic adenosine monophosphatecyclic guanosine monophosphatecyclooxygenase-2cystathionine-β-synthasecytoplasmic polyadenylation element binding proteinDHPGdihydroxyphenylglycineDNA methyltransferaseDNA methyltransferase inhibitorDNMTDNMTidorsal root ganglionDRGeEF2EIF4EEIF4E binding proteinEpigeneticERKeukaryotic elongation factor 2eukaryotic translation initiation factor 4Eextracellular receptor kinasefast conducting systemFCSFK 506 binding proteinFKBP5FMRFaHATHDACHDACiHistonehistone acetyltransferasehistone acetyltransferase E1A binding protein p300histone deacetylasehistone deacetylase inhibitorIL-6inositol 1,4,5-trisphosphateinterleukin 6intermediate-term facilitationIP3ITFlateral giant neuronLELeft E clusterLGlong-term depressionlong-term facilitationlong-term hyperexcitabilitylong-term potentiationlong-term sensitizationLTDLTFLTHLTPLTSMAPKMeCP2Methylationmethyl-CpG-binding protein 2mitogen activated protein kinaseneuron-restrictive silence factorneuron-restrictive silencer elementNF-κBnitric oxideNONRMNRSENRSFnuclear factor kappa-light-chain-enhancer of activated B cellsnucleus raphe magnusp300PARPpartial sciatic nerve ligationPGE2Pi-RNAsPiwi-interacting RNAsPKAPKCPKGPKMpoly-(ADP-ribose) polymerasepost-translational modificationspost-traumatic stress disorderPre-Met-ARg-Phe-NH(2)prostaglandin E2protein kinase Cprotein kinase Gprotein kinase MPSNLPTMPTSDS6KS6 kinaseS-adenosyl-methionineSAHASAMSensitizationserotoninserum- and glucocorticoid-inducible kinaseSGK1SGWRshort-term facilitationsiphon-gill withdrawal reflexSNISNLspared nerve injuryspinal nerve ligationSTFsuberoylanilide hydroxamic acidsulfotransferase family 1A, phenol-preferring, member 1SULT1A1target of rapamycinTORtrichostatin ATrkBTSAtyrosine kinase receptor Bubiquitin C-terminal hydrolaseUCHVCventrocaudal clusterszeta inhibitory peptideZIP

Identifiers

PMID23796633
PMCPMC3769437

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.