ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Tumor Necrosis Factor-α-Mediated Metaplastic Inhibition of LTP Is Constitutively Engaged in an Alzheimer's Disease Model.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- TNF-dependent regulation of synaptic plasticity and neuronal activity: implications for psychiatric disorders.Molecular psychiatry · 2026Review
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Virus-mediated gene transfer of soluble amyloid precursor protein-alpha via systemic injection in a mouse model of Alzheimer's disease.Gene therapy · 2026Article
- Dopamine: The Essential Bridge Mediating Obstructive Sleep Apnea and Hippocampus-Dependent Learning and Memory Impairments.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- Microglia depletion improves hippocampal circuit function after mild traumatic brain injury in male mice.Brain, behavior, and immunity · 2026Article
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- TIMP-1 enhances Akt and BDNF signaling in neurons to reduce synaptic and cognitive deficits in 5xFAD mouse model of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Sleep-Disordered Breathing and Interactions with Opioids: A Narrative Review.Journal of clinical medicine · 2025Review
- Microglia-orchestrated neuroinflammation and synaptic remodeling: roles of pro-inflammatory cytokines and receptors in neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Patient-derived tau and amyloid-β facilitate long-term depressionBrain communications · 2024Article
- Aß Pathology and Neuron-Glia Interactions: A Synaptocentric View.Neurochemical research · 2023Review
- Intermittent systemic exposure to lipopolysaccharide-induced inflammation disrupts hippocampal long-term potentiation and impairs cognition in aging male mice.Brain, behavior, and immunity · 2023Article
- mGluR-dependent plasticity in rodent models of Alzheimer's disease.Frontiers in synaptic neuroscience · 2023Article
- Dopamine and norepinephrine are embracing their immune side and so should we.Current opinion in neurobiology · 2022Review
- Article
- Pathway-specific TNF-mediated metaplasticity in hippocampal area CA1.Scientific reports · 2022Article
- Activation of dopamine D2 receptors attenuates neuroinflammation and ameliorates the memory impairment induced by rapid eye movement sleep deprivation in a murine model.Frontiers in neuroscience · 2022Article
- Article
- Broader Insights into Understanding Tumor Necrosis Factor and Neurodegenerative Disease Pathogenesis Infer New Therapeutic Approaches.Journal of Alzheimer's disease : JAD · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LTP, a fundamental mechanism of learning and memory, is a highly regulated process. One form of regulation is metaplasticity (i.e., the activity-dependent and long-lasting changes in neuronal state that orchestrate the direction, magnitude, and persistence of future synaptic plasticity). We have previously described a heterodendritic metaplasticity effect, whereby strong high-frequency priming stimulation in stratum oriens inhibits subsequent LTP in the stratum radiatum of hippocampal area CA1, potentially by engagement of the enmeshed astrocytic network. This effect may occur due to neuron-glia interactions in response to priming stimulation that leads to the release of gliotransmitters. Here we found in male rats that TNFα and associated signal transduction enzymes, but not interleukin-1β (IL-1β), were responsible for mediating the metaplasticity effect. Replacing priming stimulation with TNFα incubation reproduced these effects. As TNFα levels are elevated in Alzheimer's disease, we examined whether heterodendritic metaplasticity is dysregulated in a transgenic mouse model of the disease, either before or after amyloid plaque formation. We showed that TNFα and IL-1β levels were significantly increased in aged but not young transgenic mice. Although control LTP was impaired in the young transgenic mice, it was not TNFα-dependent. In the older transgenic mice, however, LTP was impaired in a way that occluded further reduction by heterosynaptic metaplasticity, whereas LTP was entirely rescued by incubation with a TNFα antibody, but not an IL-1β antibody. Thus, TNFα mediates a heterodendritic metaplasticity in healthy rodents that becomes constitutively and selectively engaged in a mouse model of Alzheimer's disease.
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