Evidence map›Paper›PMID 31364032›Full record

ArticleNeurotoxicity research2020

Alterations in Synaptic Plasticity and Oxidative Stress Following Long-Term Paracetamol Treatment in Rat Brain.

Laddawan Lalert, Wilawan Ji-Au, Sirinapa Srikam, Tipthanan Chotipinit, Sompol Sanguanrungsirikul, Anan Srikiatkhachorn, Supang Maneesri-le Grand

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Role ofAnnals of neurosciences · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

7 authors at 2 institutions in 1 country.

Laddawan LalertElectron Microscope Unit, Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Wilawan Ji-AuElectron Microscope Unit, Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Sirinapa SrikamElectron Microscope Unit, Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Tipthanan ChotipinitElectron Microscope Unit, Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Sompol SanguanrungsirikulDepartment of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Anan SrikiatkhachornFaculty of Medicine, King Mongkut's Institute of Technology Ladkrabang, Bangkok, 10520, Thailand.
Supang Maneesri-le GrandElectron Microscope Unit, Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand. le.grand.maneesri.s@gmail.com.
Chulalongkorn University · THKing Mongkut's Institute of Technology Ladkrabang · TH

Funding

National Research Council of Thailand NRCT, GB-B_60_074_30_18Thailand Research Fund PHD/0109/2557
6 · The paper itself

Abstract

Several studies have recently revealed that cognitive function can be affected by paracetamol (APAP) treatment. However, the exact impact of this drug treatment on learning and memory has not been clarified. This study aimed to investigate the effect of APAP treatment on the alteration of synapses and oxidative stress in the rat frontal cortex and hippocampus. APAP at a dose of 200 mg/kg bw was fed to adult male Wistar rats through either acute (n = 10), 15-day (n = 10), or 30-day (n = 10) treatment regimens. The synaptic ultrastructure and proteins, synaptophysin (SYP) and postsynaptic density-95 (PSD-95), were monitored. The amount of protein carbonyl oxidation (PCO) and glutathione (GSH) levels were examined. Our results demonstrated that acute treatment with APAP had no effect on synapses and oxidative stress. However, the synapses obtained from rats with 15-day APAP treatment showed a marked shortening of active zones and widening of the synaptic cleft. Decrement of SYP and PSD-95 proteins were demonstrated in these rats as well. With 30-day APAP treatment, the alteration of the synaptic ultrastructure and proteins was more evident. Moreover, the depletion of GSH and the elevation of PCO levels were demonstrated in the rats treated with APAP for 30 days. These results suggest that long-term APAP treatment can induce synaptic degeneration in the hippocampus and frontal cortex. The increase in oxidative stress in these brain areas may be due to the deleterious effect of this drug.

Indexed as

AcetaminophenAnalgesics, Non-NarcoticAnimalsBrainGlutathioneMaleNeuronal PlasticityOxidative StressProtein CarbonylationRatsRats, WistarSynapsesTime FactorsAcetaminophenAnalgesics, Non-NarcoticGlutathioneLong-term treatmentOxidative stressParacetamolPostsynaptic density-95Synaptic ultrastructureSynaptophysin

Identifiers

PMID31364032
OpenAlexW2965559134

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.