Evidence map›Paper›PMID 11427716›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Neurotensin-deficient mice show altered responses to antipsychotic drugs.

P R Dobner, J Fadel, N Deitemeyer, R E Carraway, A Y Deutch

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. 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, 64 citations in OpenAlex.

  1. Article
  2. Neurotensin differentially regulates bile acid metabolism and intestinal FXR-bile acid transporter axis in response to nutrient abundance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Medical sequencing at the extremes of human body mass.American journal of human genetics · 2007
    Article
  15. Corticotropin-releasing hormone induces skin vascular permeability through a neurotensin-dependent process.Proceedings of the National Academy of Sciences of the United States of America · 2006
    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

5 authors at 2 institutions in 1 country.

P R DobnerDepartment of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA 01655, USA. paul.dobner@umassmed.edu
J Fadel
N Deitemeyer
R E Carraway
A Y Deutch
University of Massachusetts Chan Medical School · USVanderbilt University Medical Center · US

Funding

MONOAMINERGIC REGULATION OF GABA AND SCHIZOPHRENIAR01MH057995 · NIMH · VANDERBILT UNIVERSITY · PI DEUTCH, ARIEL Y · 1997 to 2004
$1.4M
NEUROTENSIN GENE REGULATION IN NEURAL CREST DERIVED CELLR01HL033307 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DOBNER, PAUL RICHARD · 1988 to 1994
–
STUDIES OF NEUROTENSIN GENE STRUCTURE AND REGULATIONR23HL033307 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DOBNER, PAUL RICHARD · 1985 to 1987
–
NHLBI NIH HHS HL 33307NIMH NIH HHS MH 57995NIMH NIH HHS R01 MH057995
6 · The paper itself

Abstract

The peptide transmitter neurotensin (NT) exerts diverse neurochemical effects that resemble those seen after acute administration of antipsychotic drugs (APDs). These drugs also induce NT expression in the striatum; this and other convergent findings have led to the suggestion that NT may mediate some APD effects. Here, we demonstrate that the ability of the typical APD haloperidol to induce Fos expression in the dorsolateral striatum is markedly attenuated in NT-null mutant mice. The induction of Fos and NT in the dorsolateral striatum in response to typical, but not atypical, APDs has led to the hypothesis that the increased expression of these proteins is mechanistically related to the production of extrapyramidal side effects (EPS). However, we found that catalepsy, which is thought to reflect the EPS of typical APDs, is unaffected in NT-null mutant mice, suggesting that NT does not contribute to the generation of EPS. We conclude that NT is required for haloperidol-elicited activation of a specific population of striatal neurons but not haloperidol-induced catalepsy. These results are consistent with the hypothesis that endogenous NT mediates a specific subset of APD actions.

Indexed as

AnimalsAntipsychotic AgentsCatalepsyGene DeletionGene TargetingHaloperidolMiceMolecular Sequence DataNeurotensinAntipsychotic AgentsHaloperidolNeurotensin

Identifiers

PMID11427716
PMCPMC35465
OpenAlexW2019335735

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.