Evidence map›Paper›PMID 10729324›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Hippocampal abnormalities and enhanced excitability in a murine model of human lissencephaly.

M W Fleck, S Hirotsune, M J Gambello, E Phillips-Tansey, G Suares, R F Mervis, A Wynshaw-Boris, C J McBain

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
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  17. Microtubule plus-end tracking proteins in neuronal development.Cellular and molecular life sciences : CMLS · 2016
    Review
  18. Review
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  20. Neuronal migration and its disorders affecting the CA3 region.Frontiers in cellular neuroscience · 2014
    Review
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

8 authors at 3 institutions in 2 countries.

M W FleckLaboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
S Hirotsune
M J Gambello
E Phillips-Tansey
G Suares
R F Mervis
A Wynshaw-Boris
C J McBain
National Institutes of Health · USNational Human Genome Research Institute · USHealth and Human Development (2HD) Research Network · CM

Funding

Cellular And Synaptic Physiology Of Hippocampal InterneuronsZIAHD001205 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MCBAIN, CHRIS J. · 2009 to 2025
$45.8M
Cellular/Synaptic Physiology Of Hippocampal InterneuronsZ01HD001205 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MCBAIN, CHRIS J. · 1993 to 2008
$3.7M
6 · The paper itself

Abstract

Human cortical heterotopia and neuronal migration disorders result in epilepsy; however, the precise mechanisms remain elusive. Here we demonstrate severe neuronal dysplasia and heterotopia throughout the granule cell and pyramidal cell layers of mice containing a heterozygous deletion of Lis1, a mouse model of human 17p13.3-linked lissencephaly. Birth-dating analysis using bromodeoxyuridine revealed that neurons in Lis1+/- murine hippocampus are born at the appropriate time but fail in migration to form a defined cell layer. Heterotopic pyramidal neurons in Lis1+/- mice were stunted and possessed fewer dendritic branches, whereas dentate granule cells were hypertrophic and formed spiny basilar dendrites from which the principal axon emerged. Both somatostatin- and parvalbumin-containing inhibitory neurons were heterotopic and displaced into both stratum radiatum and stratum lacunosum-moleculare. Mechanisms of synaptic transmission were severely disrupted, revealing hyperexcitability at Schaffer collateral-CA1 synapses and depression of mossy fiber-CA3 transmission. In addition, the dynamic range of frequency-dependent facilitation of Lis1+/- mossy fiber transmission was less than that of wild type. Consequently, Lis1+/- hippocampi are prone to interictal electrographic seizure activity in an elevated [K(+)](o) model of epilepsy. In Lis1+/- hippocampus, intense interictal bursting was observed on elevation of extracellular potassium to 6.5 mM, a condition that resulted in only minimal bursting in wild type. These anatomical and physiological hippocampal defects may provide a neuronal basis for seizures associated with lissencephaly.

Indexed as

Disease Models, Animal1-Alkyl-2-acetylglycerophosphocholine EsteraseAnimalsBromodeoxyuridineCell MovementChoristomaEpilepsyGolgi ApparatusHippocampusHumansMiceMicrotubule-Associated ProteinsNervous System MalformationsNeuronsParvalbuminsSomatostatin1-Alkyl-2-acetylglycerophosphocholine EsteraseBromodeoxyuridineMicrotubule-Associated ProteinsPAFAH1B1 protein, humanPafah1b1 protein, mouseParvalbuminsSomatostatin

Identifiers

PMID10729324
PMCPMC6772237
OpenAlexW1530320970

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.