ArticleAging and disease2010
Role of TNFα Induced Inflammation in Delay Eyeblink Conditioning in Young and Aged Rats.
Article in Aging and disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 13 citations in OpenAlex.
- Impact of Sema3A Interference on Cerebellum-Dependent Motor Associative Learning and Memory.International journal of molecular sciences · 2026Article
- Mixed granulocytic airway inflammation impairs aversive learning and alters neuroimmune biomarkers in mice.Scientific reports · 2025Article
- Training on multiple days results in better learning in embedded eyeblink conditioning in young human adults.NPJ science of learning · 2025Article
- Aging triggers an upregulation of a multitude of cytokines in the male and especially the female rodent hippocampus but more discrete changes in other brain regions.Journal of neuroinflammation · 2021Article
- Neuro-Immune Cross-Talk in the Striatum: From Basal Ganglia Physiology to Circuit Dysfunction.Frontiers in immunology · 2021Review
- Correlation of cytokines, BDNF levels, and memory function in patients with opioid use disorder undergoing methadone maintenance treatment.Drug and alcohol dependence · 2018Article
- Serum Klotho, vitamin D, and homocysteine in combination predict the outcomes of Chinese patients with multiple system atrophy.CNS neuroscience & therapeutics · 2017Article
- Contra-Directional Expression of Serum Homocysteine and Uric Acid as Important Biomarkers of Multiple System Atrophy Severity: A Cross-Sectional Study.Frontiers in cellular neuroscience · 2015Article
- Modulation of learning and memory by cytokines: signaling mechanisms and long term consequences.Neurobiology of learning and memory · 2014Review
- Melatonin in the regulation of liver steatosis following prenatal glucocorticoid exposure.BioMed research international · 2014Article
- Calcium dysregulation and neuroinflammation: discrete and integrated mechanisms for age-related synaptic dysfunction.Ageing research reviews · 2013Review
- Disrupted sleep without sleep curtailment induces sleepiness and cognitive dysfunction via the tumor necrosis factor-α pathway.Journal of neuroinflammation · 2012Article
- Inhibition of soluble tumor necrosis factor ameliorates synaptic alterations and Ca2+ dysregulation in aged rats.PloS one · 2012Article
- Neuroimmunomodulation and Aging.Aging and disease · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tumor necrosis factor alpha (TNF-α) is a multifunctional proinflammatory cytokine, which is a critical inflammatory mediator involved in aging and neurodegenerative diseases of aging. Previous work has shown that diets enriched with antioxidants reduce levels of the cytokine TNF-α and improve classical eyeblink conditioning performance. Therefore we tested the hypothesis that the proinflamatory cytokine TNF-α may be a critical factor that modulates classical conditioning behavior. If increased levels of endogenous cerebellar TNF-α negatively affect performance on the eyeblink conditioning task in aged rats, then exogenous administration of TNF-α in young rats should result in an impaired acquisition and/or retention of eyeblink conditioning memory. On the other hand, the reduction or blockage of the age-related increase in cerebellar TNF-α levels in aged rats should result in an improvement in memory. Young (3 month old) F344 rats were pretreated with an intracerebellar injection of recombinant rat (rr)TNF-α or denatured (rr)TNF-α prior to eyeblink conditioning coupled to microdialysis. The results showed that young rats treated with rrTNF-α have a decreased rate of learning compared to the control group. Norepinephrine which has been shown to play a critical role in cerebellar learning tasks presented a shift on training day one of young rats resembling that observed in aged rats. In a second experiment aged (22 month old) F344 rats were pretreated with intracerebellar microinjection of anti-rat TNF-α three times a week for 4 weeks prior to eyeblink conditioning training couple to microdialysis. Aged rats showed a better performance in the conditioned responses when compared to controls. The release of norepinephrine in this group reached basal levels sooner than the control group but not as early as the young rats. The results of these experiments demonstrate a critical correlation between TNF-α and the rate of learning and the pattern of NE release during eyeblink conditioning.
Identifiers
21593991PMC3095107W1497313133What OpenQuestion holds
Registered trials
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.