Evidence map›Paper›PMID 22973010›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

LIS1 deficiency promotes dysfunctional synaptic integration of granule cells generated in the developing and adult dentate gyrus.

Robert F Hunt, Matthew T Dinday, William Hindle-Katel, Scott C Baraban

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  7. Review
  8. Article
  9. Article
  10. TheJournal of clinical medicine · 2019
    Review
  11. Article
  12. Article
  13. Ndel1 and Reelin Maintain Postnatal CA1 Hippocampus Integrity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  14. Article
  15. Article
  16. Microtubule plus-end tracking proteins in neuronal development.Cellular and molecular life sciences : CMLS · 2016
    Review
  17. Article
  18. Article
  19. Neuronal migration and its disorders affecting the CA3 region.Frontiers in cellular neuroscience · 2014
    Review
  20. 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

4 authors at 1 institution in 1 country.

Robert F HuntEpilepsy Research Laboratory, Department of Neurological Surgery, University of California, San Francisco, California 94143, USA. Robert.Huntiii@ucsf.edu
Matthew T Dinday
William Hindle-Katel
Scott C Baraban
University of California, San Francisco · US

Funding

Epileptogenesis in the Malformed BrainR01NS040272 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BARABAN, SCOTT C · 2001 to 2013
$3.5M
NINDS NIH HHS NS040272-10NINDS NIH HHS R01 NS040272
6 · The paper itself

Abstract

Type I lissencephaly, a neuronal migration disorder characterized by cognitive disability and refractory epilepsy, is often caused by heterozygous mutations in the LIS1 gene. Histopathologies of malformation-associated epilepsies have been well described, but it remains unclear whether hyperexcitability is attributable to disruptions in neuronal organization or abnormal circuit function. Here, we examined the effect of LIS1 deficiency on excitatory synaptic function in the dentate gyrus of hippocampus, a region believed to serve critical roles in seizure generation and learning and memory. Mice with heterozygous deletion of LIS1 exhibited robust granule cell layer dispersion, and adult-born granule cells labeled with enhanced green fluorescent protein were abnormally positioned in the molecular layer, hilus, and granule cell layer. In whole-cell patch-clamp recordings, reduced LIS1 function was associated with greater excitatory synaptic input to mature granule cells that was consistent with enhanced release probability at glutamatergic synapses. Adult-born granule cells that were ectopically positioned in the molecular layer displayed a more rapid functional maturation and integration into the synaptic network compared with newborn granule cells located in the hilus or granule cell layer or in wild-type controls. In a conditional knock-out mouse, induced LIS1 deficiency in adulthood also enhanced the excitatory input to granule cells in the absence of neuronal disorganization. These findings indicate that disruption of LIS1 has direct effects on excitatory synaptic transmission independent of laminar disorganization, and the ectopic position of adult-born granule cells within a malformed dentate gyrus critically influences their functional maturation and integration.

Indexed as

AgingNeuronsSynapses1-Alkyl-2-acetylglycerophosphocholine EsteraseAnimalsCerebellar NucleiClassical Lissencephalies and Subcortical Band HeterotopiasMiceMice, KnockoutMice, TransgenicMicrotubule-Associated ProteinsSynaptic Transmission1-Alkyl-2-acetylglycerophosphocholine EsteraseMicrotubule-Associated ProteinsPafah1b1 protein, mouse

Identifiers

PMID22973010
PMCPMC3752080
OpenAlexW2100361883

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.