Evidence map›Paper›PMID 18418668›Full record

ReviewCerebellum (London, England)2008

Thyrotropin-releasing hormone (TRH) in the cerebellum.

Nobuyuki Shibusawa, Koshi Hashimoto, Masanobu Yamada

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cerebellum (London, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Neuropeptides and Their Roles in the Cerebellum.International journal of molecular sciences · 2024
    Review
  3. [β-GluInternational journal of molecular sciences · 2021
    Article
  4. The Cerebellar Dopaminergic System.Frontiers in systems neuroscience · 2021
    Review
  5. Article
  6. Review
  7. Evolutionarily conserved TRH neuropeptide pathway regulates growth inProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  8. Review
  9. Article
  10. Article
  11. CEREBELLAR ATAXIA AS A PRESENTING FEATURE OF HYPOTHYROIDISM.Acta endocrinologica (Bucharest, Romania : 2005)
    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

3 authors at 1 institution in 1 country.

Nobuyuki ShibusawaDepartment of Medicine and Molecular Science, Gunma University Graduate School of Medicine, 3-39-15 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Koshi Hashimoto
Masanobu Yamada
Gunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyrotropin-releasing hormone (TRH) was originally isolated from the hypothalamus. Besides controlling the secretion of TSH from the anterior pituitary, this tripeptide is widely distributed in the central nervous system and regarded as a neurotransmitter or modulator of neuronal activities in extrahypothalamic regions, including the cerebellum. TRH has an important role in the regulation of energy homeostasis, feeding behavior, thermogenesis, and autonomic regulation. TRH controls energy homeostasis mainly through its hypophysiotropic actions to regulate circulating thyroid hormone levels. Recent investigations have revealed that TRH production is regulated directly at the transcriptional level by leptin, one of the adipocytokines that plays a critical role in feeding and energy expenditure. The improvement of ataxic gait is one of the important pharmacological properties of TRH. In the cerebellum, cyclic GMP has been shown to be involved in the effects of TRH. TRH knockout mice show characteristic phenotypes of tertiary hypothyroidism, but no morphological changes in their cerebellum. Further analysis of TRH-deficient mice revealed that the expression of PFTAIRE protein kinase1 (PFTK1), a cdc2-related kinase, in the cerebellum was induced by TRH through the NO-cGMP pathway. The antiataxic effect of TRH and TRH analogs has been investigated in rolling mouse Nagoya (RMN) or 3-acetylpyridine treated rats, which are regarded as a model of human cerebellar degenerative disease. TRH and TRH analogs are promising clinical therapeutic agents for inducing arousal effects, amelioration of mental depression, and improvement of cerebellar ataxia.

Indexed as

AnimalsBody Temperature RegulationBrainCerebellumHumansHypothalamusMiceMice, KnockoutSpinocerebellar DegenerationsThermogenesisThyrotropin-Releasing HormoneXenopus laevisThyrotropin-Releasing Hormone

Identifiers

PMID18418668
OpenAlexW1994689164

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.