Evidence map›Paper›PMID 2992787›Full record

ReviewCellular and molecular neurobiology1985

A possible mechanism of morphometric changes in dendritic spines induced by stimulation.

E Fifková

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 1985. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 38% 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

20 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
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  9. Long-term potentiation-dependent spine enlargement requires synaptic Ca2+-permeable AMPA receptors recruited by CaM-kinase I.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  10. Article
  11. A novel mechanism of dendritic spine plasticity involving estradiol induction of prostaglandin-E2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
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  17. Morphology of a sensory neuron in Drosophila is abnormal in memory mutants and changes during aging.Proceedings of the National Academy of Sciences of the United States of America · 1991
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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

1 author at 1 institution in 1 country.

E Fifková
University of Colorado Boulder · US

Funding

CHRONIC EFFECT OF ETHANOL ON THE DENTATE FASCIAR01AA006196 · NIAAA · UNIVERSITY OF COLORADO AT BOULDER · PI FIFKOVA, EVA · 1985 to 1989
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ACTIN FILAMENTS &CALCIUM IN NEURONS OF AGED RATSR01AG004804 · NIA · UNIVERSITY OF COLORADO AT BOULDER · PI FIFKOVA, EVA · 1985 to 1989
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MECHANISM OF POTENTIATION AND SHORT-TERM MEMORYR01MH027240 · NIMH · UNIVERSITY OF COLORADO AT BOULDER · PI FIFKOVA, EVA · 1985 to 1985
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NIAAA NIH HHS AA 06196-01NIA NIH HHS AG 04804-01NIMH NIH HHS MH 27240-08
6 · The paper itself

Abstract

A number of experimental procedures which induce increased electrical activity (including long-term potentiation) were shown to be accompanied by morphometric changes in dendritic spines. These changes include an enlargement of the spine head, shortening and widening of the spine stalk, and an increase in the length of synaptic apposition. A possible mechanism is suggested which takes into account specific cytological features of the spine and the existence of contractile proteins in neurons. Dendritic spines are defined as special domains of the neuron which have a unique organization of the cytoplasm. Actin filaments form a very dense network in the spine head, and they are longitudinally organized within the spine stalk. Spines were also shown to contain myosin and other actin-regulatory proteins. The high density of the actin network could explain the characteristic absence of the cytoplasmic organelles from dendritic spines. In analogy with other cells, such an actin organization indicates low levels of free cytosolic calcium. Even in the resting state, calcium levels may be unevenly distributed through the neuron, being lowest within the subplasmalemmal region. Due to the high surface-to-volume ratio in spines, the cytoplasm is formed mostly by the subplasmalemmal region. The spine apparatus or the smooth endoplasmic reticulum, which is recognized as a calcium-sequestering site in spines, may also contribute to the low calcium levels there. However, when in the stimulated spine the voltage-dependent calcium channels open, then, given the spine's high surface-to-volume ratio, the concentration of calcium may very quickly attain levels that will activate the actin-regulatory proteins and myosin and thus trigger the chain of events leading to the enlargement of the spine head and to the contraction (i.e., widening and shortening) of the spine stalk. The increased free cytosolic calcium may also activate the protein-producing system localized at the base of the spine, which, under certain conditions, could stabilize the morphometric changes of the spine.

Indexed as

Neuronal PlasticityActinsAnimalsBrainCalciumCell MembraneCytoskeletal ProteinsDendritesHippocampusIntracellular MembranesMyosinsNerve Tissue ProteinsRatsSynaptic TransmissionActinsCalciumCytoskeletal ProteinsMyosinsNerve Tissue Proteins

Identifiers

PMID2992787
PMCPMC11572857
OpenAlexW2098896251

What OpenQuestion holds

Textmetadata
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.