ArticleScientific reports2018
TNF-α increases the intrinsic excitability of cerebellar Purkinje cells through elevating glutamate release in Bergmann Glia.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- TNF-dependent regulation of synaptic plasticity and neuronal activity: implications for psychiatric disorders.Molecular psychiatry · 2026Review
- Prelimbic cortex-associated stress sensitisation and region-specific mitochondrial adaptations across preclinical approaches relevant to PTSD and depression.Neurobiology of stress · 2026Article
- Cerebellar microRNA-206 tunes Purkinje neuron firing dynamics to control sensorimotor gating.bioRxiv : the preprint server for biology · 2026Article
- Review
- Microglia surveillance is directed toward neuron activation during sustained intracortical microstimulation.Journal of neural engineering · 2026Article
- Methylprednisolone Restores Cognitive Impairment in mdx Mice by Inhibiting NF-κB/CCL5-mediated Neuroinflammation.Molecular neurobiology · 2025Article
- Growth Hormone Effects on Hypoxia-Induced Neuroinflammation in the Developing Cerebellum.International journal of molecular sciences · 2025Article
- Glial Cells and Aging: From the CNS to the Cerebellum.International journal of molecular sciences · 2025Review
- A review of the putative antiseizure and antiepileptogenic mechanisms of action for soticlestat.Epilepsia · 2025Review
- Role of cholesterol in modulating brain hyperexcitability.Epilepsia · 2025Review
- A magnetic resonance imaging and gut flora-based study of intake desire in overweight/obese type 2 diabetes mellitus patients.Frontiers in neuroscience · 2025Article
- The Neuroimmune System and the Cerebellum.Cerebellum (London, England) · 2024Review
- Engrailed-2 and inflammation convergently and independently impinge on cerebellar Purkinje cell differentiation.Journal of neuroinflammation · 2024Article
- A Human Brain-Chip for Modeling Brain Pathologies and Screening Blood-Brain Barrier Crossing Therapeutic Strategies.Pharmaceutics · 2024Article
- Estrogen-immuno-neuromodulation disorders in menopausal depression.Journal of neuroinflammation · 2024Review
- TNFR1 signaling converging on FGF14 controls neuronal hyperactivity and sickness behavior in experimental cerebral malaria.Journal of neuroinflammation · 2023Article
- Altered calcium signaling in Bergmann glia contributes to spinocerebellar ataxia type-1 in a mouse model of SCA1.Neurobiology of disease · 2023Article
- Sustained Hyperammonemia Activates NF-κB in Purkinje Neurons Through Activation of the TrkB-PI3K-AKT Pathway by Microglia-Derived BDNF in a Rat Model of Minimal Hepatic Encephalopathy.Molecular neurobiology · 2023Article
- Review
- Neuroimmune interactions with binge alcohol drinking in the cerebellum of IL-6 transgenic mice.Neuropharmacology · 2023Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
For decades, the glial function has been highlighted not only as the 'structural glue', but also as an 'active participant' in neural circuits. Here, we suggest that tumor necrosis factor α (TNF-α), a key inflammatory cytokine, alters the neural activity of the cerebellar Purkinje cells (PCs) by facilitating gliotransmission in the juvenile male rat cerebellum. A bath application of TNF-α (100 ng/ml) in acute cerebellar slices elevates spiking activity of PCs with no alterations in the regularity of PC firings. Interestingly, the effect of TNF-α on the intrinsic excitability of PCs was abolished under a condition in which the type1 TNF receptor (TNFR1) in Bergmann glia (BG) was genetically suppressed by viral delivery of an adeno-associated virus (AAV) containing TNFR1-shRNA. In addition, we measured the concentration of glutamate derived from dissociated cerebellar cortical astrocyte cultures treated with TNF-α and observed a progressive increase of glutamate in a time-dependent manner. We hypothesised that TNF-α-induced elevation of glutamate from BGs enveloping the synaptic cleft may directly activate metabotropic glutamate receptor1 (mGluR1). Pharmacological inhibition of mGluR1, indeed, prevented the TNF-α-mediated elevation of the intrinsic excitability in PCs. Taken together, our study reveals that TNF-α triggers glutamate release in BG, thereby increasing the intrinsic excitability of cerebellar PCs in a mGluR1-dependent manner.
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