Evidence map›Paper›PMID 29637287›Full record

ArticlePsychopharmacology2018

The effect of chronic stimulation of serotonin receptor type 7 on recognition, passive avoidance memory, hippocampal long-term potentiation, and neuronal apoptosis in the amyloid β protein treated rat.

Siamak Shahidi, Sara Soleimani Asl, Alireza Komaki, Nasrin Hashemi-Firouzi

Abstract read
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In one paragraph

Article in Psychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. 5-HTCNS neuroscience & therapeutics · 2025
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  6. Antioxidants (Basel, Switzerland) · 2024
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  10. Review
  11. Article
  12. Article
  13. Review
  14. Effects of Exercise on Long-Term Potentiation in Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Influence of hippocampal GABAMetabolic brain disease · 2018
    Article
  19. 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

4 authors at 1 institution in 1 country.

Siamak ShahidiNeurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Sara Soleimani AslAnatomy Department, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Alireza KomakiNeurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Nasrin Hashemi-FirouziNeurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. nhashemifirozi@yahoo.com.
Hamedan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleAlzheimer's disease (AD) is a neurodegenerative disorder characterized by memory impairment, neuronal death, and synaptic loss in the hippocampus. Long-term potentiation (LTP), a type of synaptic plasticity, occurs during learning and memory. Serotonin receptor type 7 (5-HTR7) activation is suggested as a possible therapeutic target for AD.

objectiveThe aim of the present study was to examine the effects of chronic treatment with the 5-HTR7 agonist, AS19, on cognitive function, memory, hippocampal plasticity, amyloid beta (Aβ) plaque accumulation, and apoptosis in an adult rat model of AD.

methodsAD was induced in rats using Aβ (single 1 μg/μL intracerebroventricular (icv) injection during surgery). The following experimental groups were included: control, sham-operated, Aβ + saline (1 μL icv for 30 days), and Aβ + AS19 (1 μg/μL icv for 30 days) groups. The animals were tested for cognition and memory performance using the novel object recognition and passive avoidance tests, respectively. Next, anesthetized rats were placed in a stereotaxic apparatus for electrode implantation, and field potentials were recorded in the hippocampal dentate gyrus. Lastly, brains were removed and Aβ plaques and neuronal apoptosis were evaluated using Congo red staining and TUNEL assay, respectively.

resultsAdministration of AS19 in the Aβ rats increased the discrimination index of the novel object recognition test. Furthermore, AS19 treatment decreased time spent in the dark compartment during the passive avoidance test. AS19 also enhanced both the population spike (PS) amplitude and the field excitatory postsynaptic potential (fEPSP) slope evoked potentials of the LTP components. Aβ plaques and neuronal apoptosis were decreased in the AS19-treated Aβ rats.

conclusionsThese results indicate that chronic treatment with a 5-HTR7 agonist can prevent Aβ-related impairments in cognition and memory performance by alleviating Aβ plaque accumulation and neuronal apoptosis, hence improving neuronal plasticity. AS19 may be useful as a therapeutic agent for AD.

Indexed as

Amyloid beta-PeptidesAnimalsApoptosisAvoidance LearningHippocampusLong-Term PotentiationMaleMemoryMemory DisordersNeuronsPeptide FragmentsRandom AllocationRatsRats, WistarReceptors, SerotoninRecognition, PsychologyAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsReceptors, Serotoninserotonin 7 receptorSerotonin Receptor AgonistsAlzheimer’s diseaseHippocampusLong-term potentiationMemoryRatSerotonin-7 receptor

Identifiers

PMID29637287
OpenAlexW2796715338

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.