Evidence map›Paper›PMID 28233179›Full record

ReviewHandbook of experimental pharmacology2017

Histidine Decarboxylase Knockout Mice as a Model of the Pathophysiology of Tourette Syndrome and Related Conditions.

Christopher Pittenger

Open access · greenAbstract readReview
In one paragraph

Review in Handbook of experimental pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
15.5field-weighted citation impact, top 1% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Sex Differences in Histamine Regulation of Striatal Dopamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Immunological Dysfunction in Tourette Syndrome and Related Disorders.International journal of molecular sciences · 2021
    Review
  11. Pharmacotherapeutic Strategies and New Targets in OCD.Current topics in behavioral neurosciences · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Animal models of OCD-relevant processes: an RDoC perspective.Journal of obsessive-compulsive and related disorders · 2019
    Article
  18. Association of Rare Genetic Variants in Opioid Receptors with Tourette Syndrome.Tremor and other hyperkinetic movements (New York, N.Y.) · 2019
    Article
  19. Article
  20. Merging the Pathophysiology and Pharmacotherapy of Tics.Tremor and other hyperkinetic movements (New York, N.Y.) · 2018
    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

1 author at 1 institution in 1 country.

Christopher PittengerDepartments of Psychiatry and Psychology, Yale Child Study Center, and Interdepartmental Neuroscience Program, Yale University School of Medicine, 34 Park Street, W315, New Haven, CT, 06519, USA. Christopher.pittenger@yale.edu.
Yale University · US

Funding

Histamine Regulation of the Basal Ganglia and the Pathophysiology of TicsR01NS101104 · NINDS · YALE UNIVERSITY · PI PITTENGER, CHRISTOPHER JOHN · 2017 to 2021
$2.3M
Histamine Regulation of Basal Ganglia FunctionR21MH109700 · NIMH · YALE UNIVERSITY · PI PITTENGER, CHRISTOPHER JOHN · 2016 to 2017
$404k
NIMH NIH HHS R21 MH109700NINDS NIH HHS R01 NS101104
6 · The paper itself

Abstract

While the normal functions of histamine (HA) in the central nervous system have gradually come into focus over the past 30 years, the relationship of abnormalities in neurotransmitter HA to human disease has been slower to emerge. New insight came with the 2010 description of a rare nonsense mutation in the biosynthetic enzyme histidine decarboxylase (Hdc) that was associated with Tourette syndrome (TS) and related conditions in a single family pedigree. Subsequent genetic work has provided further support for abnormalities of HA signaling in sporadic TS. As a result of this genetic work, Hdc knockout mice, which were generated more than 15 years ago, have been reexamined as a model of the pathophysiology of TS and related conditions. Parallel work in these KO mice and in human carriers of the Hdc mutation has revealed abnormalities in the basal ganglia system and its modulation by dopamine (DA) and has confirmed the etiologic, face, and predictive validity of the model. The Hdc-KO model thus serves as a unique platform to probe the pathophysiology of TS and related conditions, and to generate specific hypotheses for subsequent testing in humans. This chapter summarizes the development and validation of this model and recent and ongoing work using it to further investigate pathophysiological changes that may contribute to these disorders.

Indexed as

AnimalsDopamineHistamineHistidine DecarboxylaseHumansMiceMice, KnockoutMutationTourette SyndromeDopamineHistamineHistidine DecarboxylaseAnimal modelHistamineHistidine decarboxylaseObsessive–compulsive disorderTic disordersTourette syndrome

Identifiers

PMID28233179
PMCPMC5538774
OpenAlexW2591245062

What OpenQuestion holds

Textmetadata
LicenceTDM
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.