Evidence map›Paper›PMID 29546551›Full record

ReviewPsychopharmacology2018

The 5-HT

Mikael Tiger, Katarina Varnäs, Yoshiro Okubo, Johan Lundberg

Open access · hybridAbstract readReview
In one paragraph

Review in Psychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Mikael TigerDepartment of Clinical Neuroscience, Center for Psychiatry Research, Karolinska Institutet and Stockholm County Council, Centrum för psykiatriforskning, R5:0, Karolinska Universitetssjukhuset i Solna, -171 76, Stockholm, SE, Sweden. mikael.tiger@ki.se.ORCID http://orcid.org/0000-0001-8495-8125
Katarina VarnäsDepartment of Clinical Neuroscience, Center for Psychiatry Research, Karolinska Institutet and Stockholm County Council, Centrum för psykiatriforskning, R5:0, Karolinska Universitetssjukhuset i Solna, -171 76, Stockholm, SE, Sweden.
Yoshiro OkuboDepartment of Neuropsychiatry, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Johan LundbergDepartment of Clinical Neuroscience, Center for Psychiatry Research, Karolinska Institutet and Stockholm County Council, Centrum för psykiatriforskning, R5:0, Karolinska Universitetssjukhuset i Solna, -171 76, Stockholm, SE, Sweden.
Karolinska University Hospital · SENippon Medical School · JP

Funding

Vetenskapsrådet 523-2013-2982
6 · The paper itself

Abstract

Major depressive disorder (MDD) is the leading cause of disability worldwide. The serotonin hypothesis may be the model of MDD pathophysiology with the most support. The majority of antidepressants enhance synaptic serotonin levels quickly, while it usually takes weeks to discern MDD treatment effect. It has been hypothesized that the time lag between serotonin increase and reduction of MDD symptoms is due to downregulation of inhibitory receptors such as the serotonin 1B receptor (5-HT1BR). The research on 5-HT1BR has previously been hampered by a lack of selective ligands for the receptor. The last extensive review of 5-HT1BR in the pathophysiology of depression was published 2009, and based mainly on findings from animal studies. Since then, selective radioligands for in vivo quantification of brain 5-HT1BR binding with positron emission tomography has been developed, providing new knowledge on the role of 5-HT1BR in MDD and its treatment. The main focus of this review is the role of 5-HT1BR in relation to MDD and its treatment, although studies of 5-HT1BR in obsessive-compulsive disorder, alcohol dependence, and cocaine dependence are also reviewed. The evidence outlined range from animal models of disease, effects of 5-HT1B receptor agonists and antagonists, case-control studies of 5-HT1B receptor binding postmortem and in vivo, with positron emission tomography, to clinical studies of 5-HT1B receptor effects of established treatments for MDD. Low 5-HT1BR binding in limbic regions has been found in MDD patients. When 5-HT1BR ligands are administered to animals, 5-HT1BR agonists most consistently display antidepressant-like properties, though it is not yet clear how 5-HT1BR is best approached for optimal MDD treatment.

Indexed as

AnimalsAntidepressive AgentsBrainCase-Control StudiesDrug Delivery SystemsHumansMajor Depressive DisorderObsessive-Compulsive DisorderPositron-Emission TomographyReceptor, Serotonin, 5-HT1BSerotoninSerotonin 5-HT1 Receptor AntagonistsAntidepressive AgentsReceptor, Serotonin, 5-HT1BSerotoninSerotonin 5-HT1 Receptor Antagonists5-HT1B receptorsAntidepressantsDepressionSerotonin

Identifiers

PMID29546551
PMCPMC5919989
OpenAlexW2789328564

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.