Evidence map›Paper›PMID 17097238›Full record

ArticleNeuroscience2007

Morphology and synaptic input of substance P receptor-immunoreactive interneurons in control and epileptic human hippocampus.

K Tóth, L Wittner, Z Urbán, W K Doyle, G Buzsáki, R Shigemoto, T F Freund, Z Maglóczky

Open access · greenAbstract readComparative Study
In one paragraph

Article in Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 45% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Substance P Regulation in Epilepsy.Current neuropharmacology · 2018
    Review
  6. Review
  7. Review: Hippocampal sclerosis in epilepsy: a neuropathology review.Neuropathology and applied neurobiology · 2014
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

8 authors at 5 institutions in 3 countries.

K TóthInstitute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Szigony 43, H-1450, Budapest, Hungary.
L Wittner
Z Urbán
W K Doyle
G Buzsáki
R Shigemoto
T F Freund
Z Maglóczky
Hungarian Academy of Sciences · HUHUN-REN Institute of Experimental Medicine · HUNational Institute for Physiological Sciences · JPNew York University · USRutgers, The State University of New Jersey · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
The Hippocampal Interneuron NetworkR01MH054671 · NIMH · RUTGERS THE STATE UNIV OF NJ NEWARK · PI BUZSAKI, GYORGY · 1997 to 2017
$5.2M
NIDDK NIH HHS DK41301NIDDK NIH HHS P30 DK041301NIMH NIH HHS MH 54671NIMH NIH HHS R01 MH054671
6 · The paper itself

Abstract

Substance P (SP) is known to be a peptide that facilitates epileptic activity of principal cells in the hippocampus. Paradoxically, in other models, it was found to be protective against seizures by activating substance P receptor (SPR)-expressing interneurons. Thus, these cells appear to play an important role in the generation and regulation of epileptic seizures. The number, distribution, morphological features and input characteristics of SPR-immunoreactive cells were analyzed in surgically removed hippocampi of 28 temporal lobe epileptic patients and eight control hippocampi in order to examine their changes in epileptic tissues. SPR is expressed in a subset of inhibitory cells in the control human hippocampus, they are multipolar interneurons with smooth dendrites, present in all hippocampal subfields. This cell population is considerably different from SPR-positive cells of the rat hippocampus. The CA1 (cornu Ammonis subfield 1) region was chosen for the detailed morphological analysis of the SPR-immunoreactive cells because of its extreme vulnerability in epilepsy. The presence of various neurochemical markers identifies functionally distinct interneuron types, such as those responsible for perisomatic, dendritic or interneuron-selective inhibition. We found considerable colocalization of SPR with calbindin but not with parvalbumin, calretinin, cholecystokinin and somatostatin, therefore we suppose that SPR-positive cells participate mainly in dendritic inhibition. In the non-sclerotic CA1 region they are mainly preserved, whereas their number is decreased in the sclerotic cases. In the epileptic samples their morphology is considerably altered, they possessed more dendritic branches, which often became beaded. Analyses of synaptic coverage revealed that the ratio of symmetric synaptic input of SPR-immunoreactive cells has increased in epileptic samples. Our results suggest that SPR-positive cells are preserved while principal cells are present in the CA1 region, but show reactive changes in epilepsy including intense branching and growth of their dendritic arborization.

Indexed as

AdultAgedCell CountDendritesEpilepsyFemaleHippocampusHumansImmunohistochemistryInterneuronsMaleMicroscopy, ImmunoelectronMiddle AgedNerve Tissue ProteinsPostmortem ChangesSubstance PNerve Tissue ProteinsSubstance P

Identifiers

PMID17097238
PMCPMC2753206
OpenAlexW2036221670

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.