Evidence map›Paper›PMID 19515951›Full record

ArticleJournal of neurophysiology2009

Inhibitory inputs to hippocampal interneurons are reorganized in Lis1 mutant mice.

Daniel L Jones, Scott C Baraban

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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  7. Microtubule plus-end tracking proteins in neuronal development.Cellular and molecular life sciences : CMLS · 2016
    Review
  8. Neuronal migration and its disorders affecting the CA3 region.Frontiers in cellular neuroscience · 2014
    Review
  9. Review
  10. LIS1 deficiency promotes dysfunctional synaptic integration of granule cells generated in the developing and adult dentate gyrus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  11. Article
  12. A Cdk5-dependent switch regulates Lis1/Ndel1/dynein-driven organelle transport in adult axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  13. Article
  14. Review
  15. Article
  16. 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

2 authors at 1 institution in 1 country.

Daniel L JonesGraduate Program in Neuroscience and Epilepsy Research Laboratory, Department of Neurological Surgery, University of California, San Francisco, San Francisco, California 94143, USA. daniel.jones@ucsf.edu
Scott C Baraban
Neurological Surgery · 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 R01 NS040272NINDS NIH HHS R01 NS-40272
6 · The paper itself

Abstract

Epilepsy and brain malformation are commonly associated with excessive synaptic excitation and decreased synaptic inhibition of principal neurons. However, few studies have examined the state of synaptic inhibition of interneurons in an epileptic, malformed brain. We analyzed inhibitory inputs, mediated by gamma-aminobutyric acid (GABA), to hippocampal interneurons in a mouse model of type 1 lissencephaly, a neurological disorder linked with severe seizures and brain malformation. In the disorganized hippocampal area CA1 of Lis1(+/-) mice, we initially observed a selective displacement of fast-spiking, parvalbumin-positive basket-type interneurons from stratum oriens (SO) locations to s. radiatum and s. lacunosum-moleculare (R/LM). Next, we recorded spontaneous and miniature inhibitory postsynaptic currents (sIPSCs and mIPSCs) onto visually identified interneurons located in SO or R/LM of Lis1(+/-) mice and age-matched littermate controls. We observed significant, layer-specific reorganizations in GABAergic inhibition of interneurons in Lis1 mutant mice. Spontaneous IPSC frequency onto SO interneurons was significantly increased in hippocampal slices from Lis1(+/-) mice, whereas mIPSC mean amplitude onto these interneurons was significantly decreased. In addition, the weighted decay times of sIPSCs and mIPSCs were significantly increased in R/LM interneurons. Taken together, these findings illustrate the extensive redistribution and reorganization of inhibitory connections between interneurons that can take place in a malformed brain.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseAction PotentialsAnimalsCalbindin 2Classical Lissencephalies and Subcortical Band HeterotopiasDisease Models, Animalgamma-Aminobutyric AcidHippocampusInhibitory Postsynaptic PotentialsInterneuronsIn Vitro TechniquesMembrane PotentialsMiceMice, Mutant StrainsMicrotubule-Associated ProteinsNeural Pathways1-Alkyl-2-acetylglycerophosphocholine EsteraseCalbindin 2gamma-Aminobutyric AcidMicrotubule-Associated ProteinsPafah1b1 protein, mouseParvalbuminsS100 Calcium Binding Protein GSomatostatin

Identifiers

PMID19515951
PMCPMC2724351
OpenAlexW2101887216

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.