Evidence map›Paper›PMID 35204812›Full record

ReviewBiomolecules2022

Somatostatin and Somatostatin-Containing Interneurons-From Plasticity to Pathology.

Monika Liguz-Lecznar, Grzegorz Dobrzanski, Malgorzata Kossut

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  6. The Somatostatin Pathway Projected from the Basal Forebrain to the Lateral Habenula Promotes Isoflurane Anesthesia Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Role and mechanisms of interneurons in chronic pain and pain-induced cognitive impairment.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  11. Common and contrasting effects of 5-HTergic signaling in pyramidal cells and SOM interneurons of the mouse cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  12. Review
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  15. Article
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  18. Article
  19. Loss of mGluMolecular psychiatry · 2024
    Article
  20. 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.

Monika Liguz-LecznarNencki Institute of Experimental Biology, 3 Pasteur Str., 02-093 Warsaw, Poland.
Grzegorz DobrzanskiNencki Institute of Experimental Biology, 3 Pasteur Str., 02-093 Warsaw, Poland.
Malgorzata KossutNencki Institute of Experimental Biology, 3 Pasteur Str., 02-093 Warsaw, Poland.
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the obvious differences in the pathophysiology of distinct neuropsychiatric diseases or neurodegenerative disorders, some of them share some general but pivotal mechanisms, one of which is the disruption of excitation/inhibition balance. Such an imbalance can be generated by changes in the inhibitory system, very often mediated by somatostatin-containing interneurons (SOM-INs). In physiology, this group of inhibitory interneurons, as well as somatostatin itself, profoundly shapes the brain activity, thus influencing the behavior and plasticity; however, the changes in the number, density and activity of SOM-INs or levels of somatostatin are found throughout many neuropsychiatric and neurological conditions, both in patients and animal models. Here, we (1) briefly describe the brain somatostatinergic system, characterizing the neuropeptide somatostatin itself, its receptors and functions, as well the physiology and circuitry of SOM-INs; and (2) summarize the effects of the activity of somatostatin and SOM-INs in both physiological brain processes and pathological brain conditions, focusing primarily on learning-induced plasticity and encompassing selected neuropsychological and neurodegenerative disorders, respectively. The presented data indicate the somatostatinergic-system-mediated inhibition as a substantial factor in the mechanisms of neuroplasticity, often disrupted in a plethora of brain pathologies.

Indexed as

InterneuronsSomatostatinAnimalsHumansLearningNeuronal PlasticitySomatostatindiseaseplasticitysomatostatinsomatostatin interneurons

Identifiers

PMID35204812
PMCPMC8869243
OpenAlexW4213339408

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.