Evidence map›Paper›PMID 28044424›Full record

ArticleCNS neuroscience & therapeutics2017

Ocular Nerve Growth Factor Administration Modulates Brain-derived Neurotrophic Factor Signaling in Prefrontal Cortex of Healthy and Diabetic Rats.

Pamela Rosso, Sara De Nicolò, Valentina Carito, Marco Fiore, Angela Iannitelli, Sandra Moreno, Paola Tirassa

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Mechanism by which hyperglycemia regulates precursor of brainZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Nerve Growth Factor in Alcohol Use Disorders.Current neuropharmacology · 2021
    Review
  10. Review
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 3 institutions in 1 country.

Pamela RossoNational Research Council (CNR), Institute of Cell Biology & Neurobiology, Rome, Italy.
Sara De NicolòNational Research Council (CNR), Institute of Cell Biology & Neurobiology, Rome, Italy.
Valentina CaritoNational Research Council (CNR), Institute of Cell Biology & Neurobiology, Rome, Italy.
Marco FioreNational Research Council (CNR), Institute of Cell Biology & Neurobiology, Rome, Italy.
Angela IannitelliDepartment of Medical-Surgical Sciences and Biotechnologies, Faculty of Pharmacy and Medicine, "Sapienza" University of Rome, Rome, Italy.
Sandra MorenoDepartment of Science, LIME, University Roma Tre, Rome, Italy.
Paola TirassaNational Research Council (CNR), Institute of Cell Biology & Neurobiology, Rome, Italy.
National Research Council · ITRoma Tre University · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsNerve growth factor (NGF) eyedrops (ed-NGF) activate brain neurons, stimulate growth factors, including brain-derived neurotrophic factor (BDNF), and exert neuroprotection in the forebrain of streptozotocin-induced diabetic rats (STZ rats). In this study, the effects of ed-NGF on BDNF signaling in the prefrontal cortex (PFC) were explored in healthy and STZ-diabetic rats, in which cortical neuronal and axonal loss, and altered circulating BDNF associated with depressive phenotype are also described.

methodsSTZ and healthy (CTR) adult rats received ed-NGF twice a day for 2 weeks. Depressive phenotype was identified by force swimming test (FST). Proteins extracted from PFC were processed for ELISA and Western blot analyses to measure the expression of BDNF, proBDNF, and their receptors and intracellular signals.

resultsed-NGF treatment modulates BDNF pathway in PFC and normalizes the STZ-induced BDNF alterations by stimulating TRK-mediated survival mechanism. A decreased latency in FST was also found in STZ rats, while no change was observed comparing CTR + NGF and STZ + NGF with CTR.

conclusionThe present data confirm the capacity of ed-NGF treatment to affect brain neurons and lead to brain damage recovery by activating protective and remodeling pathways triggered by BDNF. We suggest that the ed-NGF-induced changes in BDNF signaling might influence the manifestation of depressive phenotype in diabetic rats.

Indexed as

AnimalsBody WeightBrain-Derived Neurotrophic FactorCaspase 3Depressive DisorderDiabetes Mellitus, ExperimentalDisease Models, AnimalGlutamate DecarboxylaseMaleNerve Growth FactorNeural Cell Adhesion Molecule L1Phosphopyruvate HydratasePrefrontal CortexRatsRats, Sprague-DawleyReaction TimeBrain-Derived Neurotrophic FactorCaspase 3Glutamate Decarboxylaseglutamate decarboxylase 1Nerve Growth FactorNeural Cell Adhesion Molecule L1Phosphopyruvate Hydratasepolysialyl neural cell adhesion moleculeSialic AcidsStreptozocinDepressionDiabetesNGF eyedropsp75NTRTrkB

Identifiers

PMID28044424
PMCPMC6492657
OpenAlexW2566433210

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.