The DOI matches its Crossref record; 64 of the 74 references it cites were found in a registry or an index.
Differential Regulation of AMPA Receptor and GABA Receptor Trafficking by Tumor Necrosis Factor-α
Open accessAbstract
The proinflammatory cytokine tumor necrosis factor-α (TNFα) causes a rapid exocytosis of AMPA receptors in hippocampal pyramidal cells and is constitutively required for the maintenance of normal surface expression of AMPA receptors. Here we demonstrate that TNFα acts on neuronal TNFR1 receptors to preferentially exocytose glutamate receptor 2-lacking AMPA receptors through a phosphatidylinositol 3 kinase-dependent process. This increases excitatory synaptic strength while changing the molecular stoichiometry of synaptic AMPA receptors. Conversely, TNFα causes an endocytosis of GABA A receptors, resulting in fewer surface GABA A receptors and a decrease in inhibitory synaptic strength. These results suggest that TNFα can regulate neuronal circuit homeostasis in a manner that may exacerbate excitotoxic damage resulting from neuronal insults.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This model is based on the observations that TNFa levels are elevated by prolonged (48 h) activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002;Stellwagen et al. 2005;Stellwagen and Malenka 2006).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Stellwagen et al. 2005
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This model is based on the observations that TNFa levels are elevated by prolonged (48 h) activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002;Stellwagen et al. 2005;Stellwagen and Malenka 2006).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Stellwagen et al. 2005
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This model is based on the observations that TNFa levels are elevated by prolonged (48 h) activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002;Stellwagen et al. 2005;Stellwagen and Malenka 2006).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Stellwagen et al. 2005
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The Glutamate Receptor Ion Channels
Dingledine, R., Borges, K., Bowie, D., & Traynelis, S. F. (1999) · Pharmacological Reviews · doi:10.1016/s0031-6997(24)01394-2 · Cited by 3,554 · cited 9×
“These new synaptic AMPARs are likely replaced over time by GluR2-containing receptors, because HPP-spermine had no effect on mEPSCs recorded from control neurons despite the finding that constitutive TNF release is necessary to maintain normal levels of surface AMPARs.”
BackgroundInfluentialAMPA Receptor Trafficking and Synaptic Plasticity
Malinow, R., & Malenka, R. C. (2002) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.25.112701.142758 · Cited by 2,588 · cited 2×
“Trafficking of these receptors is thought to underlie, at least in part, both rapid forms of synaptic plasticity and slower homeostatic changes in transmission (Malinow and Malenka, 2002; Turrigiano and Nelson, 2004).”
BackgroundSelf-citationHomeostatic plasticity in the developing nervous system
Turrigiano, G. G., & Nelson, S. B. (2004) · Nature Reviews Neuroscience · doi:10.1038/nrn1327 · Cited by 2,485 · cited 9×
“…circuit activity is pharmacologically reduced, excitatory synapses are strengthened and inhibitory synapses weakened (Turrigiano and Nelson, 2004), at least in part through changes in the synaptic surface expression of AMPARs and GABAA receptors (Kilman et al., 2002; Turrigiano and Nelson, 2004).”
BackgroundResultInfluentialSignal transduction by tumor necrosis factor and its relatives.
Baud, V., & Karin, M. (2001) · Trends in Cell Biology · doi:10.1016/s0962-8924(01)02064-5 · Cited by 1,741 · cited 3×
“TNFR1 initiates signaling through an array of downstream pathways, most known for their roles in gene expression and apoptosis (Pan et al., 1997; Baud and Karin, 2001).”
BackgroundControl of Synaptic Strength by Glial TNFα
Beattie, E. C., Stellwagen, D., Morishita, W., Bresnahan, J. C., Ha, B. K., Von Zastrow, M., Beattie, M. S., & Malenka, R. C. (2002) · Science · doi:10.1126/science.1067859 · Cited by 1,344 · cited 7×
“Recently, the proinflammatory cytokine tumor necrosis factor- (TNF ) was found to be a novel, gliareleased factor that increases the surface expression of AMPARs (Beattie et al., 2002).”
BackgroundMethodResultInfluentialSelf-citationBezzi, P., Domercq, M., Brambilla, L., Galli, R., Schols, D., De Clercq, E., Vescovi, A., Bagetta, G., Kollias, G., Meldolesi, J., et al. (2001) · Nature Neuroscience · doi:10.1038/89490 · Cited by 1,102 · cited 2×
“In contrast, consistent with our previous results (Beattie et al., 2002), a recombinant soluble form of the TNF receptor TNFR1 (sTNFR), which binds endogenous TNF (Bezzi et al., 2001), decreased surface GluR1 staining (10 g/ ml; 72 5%; n 59) (Fig.”
BackgroundResultReinsertion or Degradation of AMPA Receptors Determined by Activity-Dependent Endocytic Sorting
Ehlers, M. D. (2000) · Neuron · doi:10.1016/s0896-6273(00)00129-x · Cited by 1,096 · cited 2×
“It is possible that the antibodies to GluR1 might somehow sterically inhibit antibody staining of surface GluR2, and, therefore, we used an alternative technique, biotinylation of surface AMPARs (Ehlers, 2000; Kim and von Zastrow, 2003), to reexamine whether GluR2 surface expression was increased by TNF .”
MethodGlial activation: a driving force for pathological pain
Watkins, L. R., Milligan, E. D., & Maier, S. F. (2001) · Trends in Neurosciences · doi:10.1016/s0166-2236(00)01854-3 · Cited by 1,091 · cited 1×
“Similarly, the effects of TNF could contribute to the modification of circuit behavior that underlies the hyperalgesia after peripheral nerve damage, a neuropathological state that involves glia-released cytokines, including TNF (Watkins et al., 2001; Milligan et al., 2003).”
BackgroundLu, W.-Y., Man, H., Ju, W. H., Trimble, W. S., MacDonald, J. F., & Wang, Y. T. (2001) · Neuron · doi:10.1016/s0896-6273(01)00194-5 · Cited by 935 · cited 1×
“However, glycine treatment caused an increase in surface expression of both GluR1 and GluR2 (Lu et al., 2001; Man et al., 2003), although we observed a large increase in surface GluR1 with TNF but no significant change in surface GluR2.”
BackgroundTumor Necrosis Factor-α: A Mediator of Focal Ischemic Brain Injury
Barone, F. C., Arvin, B., White, R. F., Miller, A., Webb, C. L., Willette, R. N., Lysko, P. G., & Feuerstein, G. Z. (1997) · Stroke · doi:10.1161/01.str.28.6.1233 · Cited by 863 · cited 2×
“…Nagatsu et al., 2000; Perry et al., 2001), and preventing its signaling in vivo can, for example, prevent or reduce neuron loss after cerebral ischemia (Dawson et al., 1996; Barone et al., 1997; Meistrell et al., 1997) and head injury (for review, see Barone et al., 1997; Shohami et al., 1999).”
Research works printed but not linked: 8
- 1999, Pharmacol Rev, 51, 7
- Goslin K, Asmussen H, Banker G (1998) Rat hippocampal neurons in lowdensity culture. In: Culturing nerve cells (Goslin K, Banker G, eds), pp 339-370. Cambridge, MA: MIT. · DOI
- 10.1073/pnas.050586497 · DOI
- 1997, Shock, 8, 341
- 2000, J Neural Transm Suppl, 58, 143
- 10.1080/13550280290101021 · DOI
- 2002, Adv Exp Med Biol, 513, 87
- 2003, Soc Neurosci Abstr, 29, 10
Cited by
Sorted by citations
Items 401–500 of 831
Baune, B. T. (2016) · Current topics in behavioral neurosciences · doi:10.1007/7854_2016_19 · Cited by 47
“Pro-inflammatory cytokines induce gene expression and synthesis of corticotrophin releasing factor (CRF), which stimulates adrenocorticotropic hormone (ACTH) release and causes glucocorticoid secretion [19].”
BackgroundRole of interleukin-10 (IL-10) in regulation of GABAergic transmission and acute response to ethanol
Suryanarayanan, A., Carter, J. M., Landin, J. D., Morrow, A. L., Werner, D. F., & Spigelman, I. (2016) · Neuropharmacology · doi:10.1016/j.neuropharm.2016.03.027 · Cited by 36
(Re)building the nervous system: A review of neuron–glia interactions from development to disease
Demmings, M. D., Chagas, L. D. S., Traetta, M. E., Rodrigues, R. S., Acutain, M. F., Barykin, E. P., Datusalia, A. K., German‐Castelan, L., Mattera, V. S., Mazengenya, P., et al. (2024) · Journal of Neurochemistry · doi:10.1111/jnc.16258 · Cited by 44
“…α ), ATP, or brain-derived neurotrophic factor (BDNF), microglia contribute to neuronal excitability, partaking in the reorganization of synaptic receptors in neurons and glutamate release by astrocytes (Parkhurst et al., 2013; Pascual et al., 2012; Santello et al., 2011; Stellwagen et al., 2005 ).”
Microglial Cytokines Mediate Plasticity Induced by 10 Hz Repetitive Magnetic Stimulation
Eichler, A., Kleidonas, D., Turi, Z., Fliegauf, M., Kirsch, M., Pfeifer, D., Masuda, T., Prinz, M., Lenz, M., & Vlachos, A. (2023) · Journal of Neuroscience · doi:10.1523/jneurosci.2226-22.2023 · Cited by 56
“Specifically, TNFa and IL6 have been implicated as important secreted factors that modulate synaptic transmission (Furukawa and Mattson, 1998; Stellwagen et al., 2005; Garcia-Oscos et al., 2012) and plasticity (Heir and Stellwagen, 2020).”
BackgroundNeuroimmune System as a Driving Force for Plasticity Following CNS Injury
O’Reilly, M. L., & Tom, V. J. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.00187 · Cited by 44
“…surface (Serantes et al., 2006; Stück et al., 2012), yet activation of these cytokines has also been shown to suppress post-synaptic GABA receptor activation and decrease inhibitory synaptic strength (Stellwagen et al., 2005; Kawasaki et al., 2008; Pribiag and Stellwagen, 2013; Yan et al., 2015).”
BackgroundInfluentialMicroglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
Victor, T. R., & Tsirka, S. E. (2020) · Neuroimmunology and Neuroinflammation · doi:10.20517/2347-8659.2020.02 · Cited by 35
“Like IL-1β, TNF-α also affects GABA levels by increasing GABA receptor endocytosis, reducing its inhibitory action[78].”
BackgroundThe impact of inflammation on neurocognition and risk for psychosis: a critical review
Kogan, S., Ospina, L. H., Mittal, V. A., & Kimhy, D. (2019) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-019-01073-2 · Cited by 38
“Though a full discussion is beyond the scope of this review, TNF-α signaling has also been implicated in numerous ion-channel pathways involved in schizophrenia and other psychiatric disorders including in α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) channel expression, as well as glutamate [49], NMDA [50…”
BackgroundStem Cell–Based Immunomodulation After Stroke
Boshuizen, M. C. S., & Steinberg, G. K. (2018) · Stroke · doi:10.1161/strokeaha.117.020465 · Cited by 46
“synaptic plasticity by regulating neuronal surface expression of excitatory α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and inhibitory gamma-aminobutyric acid a receptors.(71,72)”
BackgroundChanana, P., & Kumar, A. (2016) · Frontiers in Neuroscience · doi:10.3389/fnins.2016.00084 · Cited by 39
Targeting tumour necrosis factor-α in hypoxia and synaptic signalling
O'Connor, J. J. (2013) · Irish Journal of Medical Science (1971 -) · doi:10.1007/s11845-013-0911-4 · Cited by 37
Blaylock, R., & Maroon, J. (2012) · Surgical neurology international · doi:10.4103/2152-7806.92935 · Cited by 37
“[135] Furthermore, recent studies have demonstrated higher concentrations of GluR2-lacking, calcium permeable AMPA receptors in CNS injury, strokes, seizures, and neurodegenerative disorders, such as ALS, PD, and AD.[154,226]”
BackgroundInfluentialTobinick, E. L. (2012) · Current Alzheimer Research · doi:10.2174/156720512799015073 · Cited by 34
“Modulation of synaptic function by TNF, including modulation of synaptic function across neuronal networks, has been established [132-136].”
BackgroundKorgaonkar, A. A., Li, Y., Sekhar, D., Subramanian, D., Guevarra, J., Swietek, B., Pallottie, A., Singh, S., Kella, K., Elkabes, S., et al. (2020) · Annals of Neurology · doi:10.1002/ana.25698 · Cited by 36
“This could occur from exocytosis and surface expression of a reserve pool of GluA1, similar to the processes mediated by glia-derived TNFα in culture systems.(64) Increases in granule cell CPAMPARs have been shown to contribute to excitotoxic damage after experimental stroke,(34) suggesting that an increase in CP-AMPA…”
ResultEvonuk, K. S., Doyle, R. E., Moseley, C. E., Thornell, I. M., Adler, K., Bingaman, A. M., Bevensee, M. O., Weaver, C. T., Min, B., & DeSilva, T. M. (2020) · Science Advances · doi:10.1126/sciadv.aax5936 · Cited by 49
Chen, Y.-C., Zhu, G.-Y., Wang, X., Shi, L., Jiang, Y., Zhang, X., & Zhang, J.-G. (2017) · Brain Research · doi:10.1016/j.brainres.2016.12.020 · Cited by 36
Epilepsy and vitamin D: a comprehensive review of current knowledge
Yazdi, S. A. M., Abbasi, M., & Yazdi, S. M. M. (2016) · Reviews in the Neurosciences · doi:10.1515/revneuro-2016-0044 · Cited by 39
“After the release of neurotransmitters from presynaptic neurons, neu rotransmitters like glutamate and γamino butyric acid (GABA) attach to their postsynaptic membra nous receptors and activate a cascade of intracellular events and changes simultaneously the confirma tion of the receptor and creates a membranous pore,…”
BackgroundInfluentialConverging Mechanisms of Epileptogenesis and Their Insight in Glioblastoma
Hills, K., Kostarelos, K., & Wykes, R. C. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.903115 · Cited by 44
Emerging Role of Microglia-Mediated Neuroinflammation in Epilepsy after Subarachnoid Hemorrhage
Wang, J., Liang, J., Deng, J., Liang, X., Wang, K., Wang, H., Qian, D., Long, H., Yang, K., & Qi, S. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02288-y · Cited by 39
Astrocytic Factors Controlling Synaptogenesis: A Team Play
Fossati, G., Matteoli, M., & Menna, E. (2020) · Cells · doi:10.3390/cells9102173 · Cited by 46
Viral Triggers and Inflammatory Mechanisms in Pediatric Epilepsy
Bartolini, L., Libbey, J. E., Ravizza, T., Fujinami, R. S., Jacobson, S., & Gaillard, W. D. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1215-5 · Cited by 34
SPARC and GluA1-Containing AMPA Receptors Promote Neuronal Health Following CNS Injury
Jones, E. V., Bernardinelli, Y., Zarruk, J. G., Chierzi, S., & Murai, K. K. (2018) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2018.00022 · Cited by 39
“We used a protocol described previously (Stellwagen et al., 2005; Jones et al., 2011) to visualize surface GluA1 and GluA2containing AMPARs under non-permeabilizing conditions.”
MethodAlterations of functional properties of hippocampal networks following repetitive closed-head injury
Logue, O. C., Cramer, N., Xu, X., Perl, D. P., & Galdzicki, Z. (2015) · Experimental Neurology · doi:10.1016/j.expneurol.2015.12.019 · Cited by 33
Procalcitonin and mortality in status epilepticus: an observational cohort study
Sutter, R., Valença, M., Tschudin-Sutter, S., Rüegg, S., & Marsch, S. (2015) · Critical Care · doi:10.1186/s13054-015-1072-9 · Cited by 35
“In addition, neurons and glial cells may express functional cytokine receptors in vitro [46, 47] and in vivo [48], underscoring that both the immune system and the central nervous system have a bidirectional influence on each other.”
BackgroundLate blocking of peripheral TNF-α is ineffective after spinal cord injury in mice.
Vidal, P., Lemmens, E., Geboes, L., Vangansewinkel, T., Nelissen, S., & Hendrix, S. (2013) · Immunobiology · doi:10.1016/j.imbio.2012.05.007 · Cited by 35
Neural-Immune Interactions in Brain Function and Alcohol Related Disorders
Cui, C., Noronha, A., & Grandison, L. (2012) · Springer eBooks · doi:10.1007/978-1-4614-4729-0 · Cited by 54
Microglia in neuroimmunopharmacology and drug addiction
Li, H., Watkins, L. R., & Wang, X. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02443-6 · Cited by 44
“3) [123, 124].”
Kodali, M., Madhu, L. N., Reger, R. L., Milutinovic, B. S., Upadhya, R., Attaluri, S., Shuai, B., Shankar, G., & Shetty, A. K. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1185883 · Cited by 39
Can glial cells save neurons in epilepsy?
Nobili, P., Nikolic, L. M., Shen, W., & Pristov, J. B. (2022) · Neural Regeneration Research · doi:10.4103/1673-5374.360281 · Cited by 35
“Indeed, it has been shown that TNFα can inhibit glutamate uptake and increase microglial glutamate release by acting on glutaminase and GJ regulation (Takeuchi et al., 2006), as well as reduce GABAergic transmission by increasing GABA receptor endocytosis (Stellwagen et al., 2005).”
BackgroundWegrzyn, D., Freund, N., Faissner, A., & Juckel, G. (2021) · Frontiers in Synaptic Neuroscience · doi:10.3389/fnsyn.2021.637549 · Cited by 37
“Surprisingly, it has been unraveled that neurons express many functional cytokine receptors and respond to the release of microglial immune factors (Viviani et al., 2003; Stellwagen et al., 2005; Gardoni et al., 2011; Vezzani and Viviani, 2015).”
BackgroundDysregulated long non-coding RNAs in the temporal lobe epilepsy mouse model
Jang, Y., Moon, J., Lee, S., Jun, J. S., Lim, J., Lim, J., Park, B.-S., Yu, J.-S., Park, D.-K., Yang, A. R., et al. (2018) · Seizure · doi:10.1016/j.seizure.2018.04.010 · Cited by 38
(Putative) sex differences in neuroimmune modulation of memory
Tronson, N. C., & Collette, K. M. (2016) · Journal of Neuroscience Research · doi:10.1002/jnr.23921 · Cited by 36
“TNFa increases glutamatergic and decreases GABAergic receptor trafficking (Beattie et al., 2002; Stellwagen, 2005), thereby impairing plasticity.”
BackgroundVitamin D3 for the Treatment of Epilepsy: Basic Mechanisms, Animal Models, and Clinical Trials
Pendo, K., & DeGiorgio, C. M. (2016) · Frontiers in Neurology · doi:10.3389/fneur.2016.00218 · Cited by 39
“The TNF-α cytokine acts as a proconvulsant because it initiates both the recruitment of AMPA receptors to the neuronal membrane and the endocytosis of GABAA receptors away from the membrane (46, 47).”
BackgroundInsights into inflammation and epilepsy from the basic and clinical sciences
Silveira, G., de Oliveira, A. C. P., & Teixeira, A. L. (2012) · Journal of Clinical Neuroscience · doi:10.1016/j.jocn.2011.10.011 · Cited by 33
The ubiquitin–proteasome system postsynaptically regulates glutamatergic synaptic function
Haas, K. F., Miller, S. L., Friedman, D. B., & Broadie, K. S. (2007) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2007.02.002 · Cited by 34
“Similarly, in mammalian CNS glutamatergic synapses, there are many examples of differential regulation of AMPA GluR subtypes occurring in physiological and pathological processes (Ogoshi and Weiss, 2003;Stellwagen et al., 2005;Thiagarajan et al., 2005;Gardner et al., 2005;Brooks-Kayal, 2005).”
BackgroundNeural dysregulation in post-COVID fatigue
Baker, A. M. E., Maffitt, N. J., Vecchio, A. D., McKeating, K. M., Baker, M. R., Baker, S. N., & Soteropoulos, D. S. (2023) · Brain Communications · doi:10.1093/braincomms/fcad122 · Cited by 38
“in the brain, that are elevated following an infection, can have profound effects on neuroplasticity.(43,44) Before being able to address whether such a mechanism operates in pCF, we first need to know which neural systems are affected.”
BackgroundToll-Like Receptor 4 Signaling and Drug Addiction
Wu, R., & Li, J. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.603445 · Cited by 36
“TNFα is shown to regulate synaptic transmission by affecting the activity of GABAA receptors, AMPA receptors and presynaptic metabotropic glutamate receptors (Bezzi et al., 2001; Stellwagen et al., 2005; Domercq et al., 2006; Stellwagen and Malenka, 2006; Pascual et al., 2012; Lewitus et al., 2014).”
BackgroundItoh, K., Taniguchi, R., Matsuo, T., Oguro, A., Vogel, C. F. A., Yamazaki, T., & Ishihara, Y. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.134363 · Cited by 36
Mashhadizadeh, S., Farbood, Y., Dianat, M., Khodadadi, A., & Sarkaki, A. (2017) · Europe PMC (PubMed Central) · doi:10.22038/ijbms.2017.8581 · Cited by 31
Wall, A. M., Mukandala, G., Greig, N. H., & O'Connor, J. J. (2015) · Journal of Neuroscience Research · doi:10.1002/jnr.23540 · Cited by 35
“The modulation of synaptic signaling by TNF-a is thought to occur via the activation of TNF R1 and R2 receptors (TNFR1 and TNFR2) on both the pre- and postsynaptic membranes of neurons and glia (Marchetti et al., 2004; Belarbi et al., 2012).”
BackgroundInfluentialSynapse Dysfunctions in Multiple Sclerosis
Schwarz, K., & Schmitz, F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24021639 · Cited by 36
Neuro-Immune Cross-Talk in the Striatum: From Basal Ganglia Physiology to Circuit Dysfunction
Mancini, A., Ghiglieri, V., Parnetti, L., Calabresi, P., & Filippo, M. D. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.644294 · Cited by 38
Perinatal Brain Injury and Inflammation: Lessons from Experimental Murine Models
Leavy, A., & Jimenez-Mateos, E. M. (2020) · Cells · doi:10.3390/cells9122640 · Cited by 39
“Similarly, another pro-inflammatory cytokine, TNFα, increases AMPA-receptor density on the membrane, contributing to the hyper-excitability [14].”
BackgroundBañuelos‐Cabrera, I., Valle-Dorado, M. G., Aldana, B. I., Orozco-Suárez, S. A., & Rocha, L. (2014) · Archives of Medical Research · doi:10.1016/j.arcmed.2014.11.010 · Cited by 36
Ouyang, H., Liu, S., Zeng, W., Levitt, R. C., Candiotti, K. A., & Hao, S. (2012) · The Scientific World JOURNAL · doi:10.1100/2012/940613 · Cited by 31
Rainey‐Smith, S. R., Andersson, D. A., Williams, R. J., & Rattray, M. (2010) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2010.06634.x · Cited by 30
“In motor neurones, using immunofluorescence with antibodies directed against intracellular domains, we detected abundant GluR1 and GluR2 with little observable GluR3 and GluR4 (Fig.”
BackgroundInfluentialTNFα in MS and Its Animal Models: Implications for Chronic Pain in the Disease
Maguire, A. D., Bethea, J. R., & Kerr, B. J. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.780876 · Cited by 33
“TNFα produced in response to inflammation can increase excitatory synapse strength and decrease inhibitory synapse strength by altering AMPA and GABAA receptor surface expression on neurons (85).”
BackgroundEngel, T., Smith, J., & Alves, M. (2021) · Journal of Inflammation Research · doi:10.2147/jir.s287740 · Cited by 36
Tukhovskaya, E. A., Turovsky, E., Turovskaya, M. V., Levin, S. G., Murashev, A., Zinchenko, V., & Godukhin, O. (2014) · Neuroscience Letters · doi:10.1016/j.neulet.2014.04.046 · Cited by 31
Nygård, M., Lundkvist, G., Hill, R., & Kristensson, K. (2009) · NeuroReport · doi:10.1097/wnr.0b013e32831f1ca2 · Cited by 31
Grünewald, B., Wickel, J., Hahn, N., Rahmati, V., Rupp, H., Chung, H., Haselmann, H., Strauß, A., Schmidl, L., Hempel, N., et al. (2024) · Molecular Therapy · doi:10.1016/j.ymthe.2024.05.001 · Cited by 32
Yao, P., Wang, S.-K., Chen, S., Xin, W., Liu, X., & Zang, Y. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.04.012 · Cited by 33
Okada, M., Fukuyama, K., Shiroyama, T., & Ueda, Y. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20153727 · Cited by 31
“These results suggest that the stimulatory effects of IFNγ are predominantly associated with the IP3-R system rather than AMPA-R [8], whereas those of TNFα are predominantly associated with AMPA-R.”
BackgroundInfluentialCampos‐Bedolla, P., Feria-Romero, I. A., & Orozco-Suárez, S. A. (2022) · Epilepsia Open · doi:10.1002/epi4.12590 · Cited by 32
Peripheral blood mononuclear cell activation sustains seizure activity
Librizzi, L., Verde, D. V., Colciaghi, F., Deleo, F., Regondi, M. C., Costanza, M., Cipelletti, B., & Curtis, M. (2021) · Epilepsia · doi:10.1111/epi.16935 · Cited by 29
Altered Blood Biomarker Profiles in Athletes with a History of Repetitive Head Impacts
Battista, A. P. D., Rhind, S. G., Richards, D. W., Churchill, N. W., BAKER, A. J., & Hutchison, M. G. (2016) · PLoS ONE · doi:10.1371/journal.pone.0159929 · Cited by 62
Li, C., Yan, Y., Cheng, J., Xiao, G., Gu, J., Zhang, L., Yuan, S., Wang, J., Shen, Y., & Zhou, Y. (2016) · Neuroscience Bulletin · doi:10.1007/s12264-016-0015-z · Cited by 33
“These cytokines, such as tumor necrosis factor-a and interleukin-1b, not only exert their excitatory effects via upregulating excitatory synaptic transmission [30, 31], but also regulate neuronal functions via interacting with modulatory systems [32].”
BackgroundHuie, J. R., Stück, E. D., Lee, K. H., Irvine, K., Beattie, M. S., Bresnahan, J. C., Grau, J. W., & Ferguson, A. R. (2015) · eNeuro · doi:10.1523/eneuro.0091-15.2015 · Cited by 29
“Prior in vitro studies revealed that TNF drives AMPAR currents, specifically by increasing synaptic GluA2-lacking CP-AMPAR expression (Beattie et al., 2002; Stellwagen et al., 2005; Leonoudakis et al., 2008).”
BackgroundLeinders, M., Koehrn, F., Bartok, B., Boyle, D., Shubayev, V., Kalcheva, I., Yu, N.-K., Park, J., Kaang, B., Hefferan, M., et al. (2014) · Pain · doi:10.1016/j.pain.2014.03.003 · Cited by 29
“This process is essential to long-term potentiation [45].”
Open study of pranlukast add-on therapy in intractable partial epilepsy.
Takahashi, Y., Imai, K., Ikeda, H., Kubota, Y., Yamazaki, E., & Susa, F. (2013) · Brain & development (Tokyo. 1979) · doi:10.1016/j.braindev.2012.04.001 · Cited by 29
“High concentrations of TNFa have been shown to increase excitotoxic death of neurons by increasing synaptic AMPA receptors and decreasing GABA receptors [27], and cause spasms in TNFa transgenic mice [28].”
Backgroundregenerative-loop potentiation of glutamate synaptic transmission by microglia and astrocytes
Bennett, M. R., Farnell, L., & Gibson, W. G. (2009) · Journal of Theoretical Biology · doi:10.1016/j.jtbi.2009.07.024 · Cited by 28
“Whether P2X7 receptors are normally present on astrocytes is unclear: compare Jabs et al. (2007), Rappold et al. (2006) and Yu et al. (2008) with Suadicani et al. (2006), Duan et al. (2003) and Ballerini et al. (1996).”
BackgroundNeural–immune interactions in disorders of sleep-wakefulness organization
Bentivoglio, M., & Kristensson, K. (2007) · Trends in Neurosciences · doi:10.1016/j.tins.2007.09.004 · Cited by 31
Okada, M., Fukuyama, K., Shiroyama, T., & Ueda, Y. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111462 · Cited by 28
Martin, S. P., & Leeman-Markowski, B. A. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2023.1287545 · Cited by 30
“AMPA-GluR1 and GluR2 receptors are also down-regulated in response to injury (21–23, 49, 114–116).”
BackgroundTurhan, L., Batmaz, S., Koçbıyık, S., & Soygur, A. H. (2016) · Nordic Journal of Psychiatry · doi:10.3109/08039488.2015.1122079 · Cited by 29
Brainstem Control of the Gastric Function
Rogers, R., & Hermann, G. (2012) · Elsevier eBooks · doi:10.1016/b978-0-12-382026-6.00031-2 · Cited by 28
Regulation of excitation by GABA(A) receptor internalization.
Leidenheimer, N. (2008) · Results and problems in cell differentiation · doi:10.1007/400_2007_039 · Cited by 28
Ruffolo, G., Alfano, V., Romagnolo, A., Zimmer, T., Mills, J. D., Cifelli, P., Gaeta, A., Morano, A., Anink, J., Mühlebner, A., et al. (2022) · Scientific Reports · doi:10.1038/s41598-022-22806-9 · Cited by 27
Oxytocin and microglia in the development of social behaviour
Gonzalez, A. M., & Hammock, E. A. D. (2022) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2021.0059 · Cited by 32
Leone, P., Mincheva, G., Balzano, T., Malaguarnera, M., Felipo, V., & Llansola, M. (2022) · Biomedicines · doi:10.3390/biomedicines10061263 · Cited by 30
Neuronal Glial Crosstalk: Specific and Shared Mechanisms in Alzheimer’s Disease
Chavda, V. K., Singh, K., Patel, V., Mishra, M., & Mishra, A. K. (2022) · Brain Sciences · doi:10.3390/brainsci12010075 · Cited by 29
“Therefore, TNF-α plays a significant role in stimulating synapses activators and leads to maximum neural activity [25,117].”
Astrocyte and Neuronal Plasticity in the Somatosensory System
Sims, R. E., Butcher, J. B., Parri, H. R., & Glazewski, S. (2015) · Neural Plasticity · doi:10.1155/2015/732014 · Cited by 28
“Scaling was observed in variety of brain areas both in vitro and in vivo including the visual cortex where open eye potentiation, induced by monocular deprivation, is dependent on TNF-α and GluR1 [25–33].”
BackgroundAalbers, M., Rijkers, K., Majoie, H., Dings, J., Schijns, O., Schipper, S., Baets, M. D., Kessels, A., Vles, J., & Hoogland, G. (2014) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2014.03.016 · Cited by 27
“(Kamikawa et al., 1998; Hu et al., 2000; Bezzi et al., 2001; Stellwagen et al., 2005), alter receptor functioning (Balosso et al.”
BackgroundLevin, S. G., & Godukhin, O. V. (2011) · Experimental Neurology · doi:10.1016/j.expneurol.2011.09.004 · Cited by 26
Pro-inflammatory cytokines modify neuronal nicotinic acetylcholine receptor assembly
Gahring, L. C., Days, E., Kaasch, T., de Mendoza, M. G., Owen, L. A., Persiyanov, K., & Rogers, S. W. (2005) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2005.05.007 · Cited by 26
“First, because IL-1h or TNFa are expressed normally by cells of the brain, and receptors for these cytokines are prevalent on most cells of the nervous system including neurons (Allan and Rothwell, 2001; Dziewulska and Mossakowski, 2003), there is a suggested role for cytokines in modulating normal cell–cell communica…”
BackgroundNeuroimmune Biomarkers in Mental Illness
Herron, J. W., Nerurkar, L., & Cavanagh, J. (2018) · Current topics in behavioral neurosciences · doi:10.1007/7854_2018_45 · Cited by 35
Neuroinflammation and Tinnitus
Shulman, A., Wang, W., Luo, H., Bao, S., Searchfield, G. D., & Zhang, J. (2021) · Current topics in behavioral neurosciences · doi:10.1007/7854_2021_238 · Cited by 37
Lenz, M., Eichler, A., Kruse, P., Strehl, A., Rodriguez-Rozada, S., Goren, I., Yogev, N., Frank, S., Waisman, A., Deller, T., et al. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.614509 · Cited by 30
Cyclooxygenase Inhibition Safety and Efficacy in Inflammation-Based Psychiatric Disorders
Perrone, M. G., Centonze, A., Miciaccia, M., Ferorelli, S., & Scilimati, A. (2020) · Molecules · doi:10.3390/molecules25225388 · Cited by 31
“In particular, pro-inflammatory cytokines induce gene expression and synthesis of corticotrophin-releasing hormone (CRH) which in turn stimulates the release of adrenocorticotropic hormone (ACTH) and causes glucocorticoid secretion [73,92].”
BackgroundWhiten, D. R., Brownjohn, P. W., Moore, S., De, S., Strano, A., Zuo, Y., Haneklaus, M., Klenerman, D., & Livesey, F. J. (2020) · Brain Communications · doi:10.1093/braincomms/fcaa146 · Cited by 28
“It has been demonstrated that TNFR1 signalling can modulate synaptic strength via exocytosis of AMPA receptors (Beattie et al., 2002; Stellwagen et al., 2005), and endocytosis of GABA receptors (Stellwagen et al.”
BackgroundLi, T., Jia, Y., Wang, Q., Shao, X.-Q., Zhang, P., & Lv, R. (2018) · Brain Research · doi:10.1016/j.brainres.2018.07.013 · Cited by 32
Becker, D., Deller, T., & Vlachos, A. (2015) · Scientific Reports · doi:10.1038/srep12726 · Cited by 28
Markus, T., Cronberg, T., Cilio, C., Pronk, C., Wieloch, T., & Ley, D. (2009) · Journal of Cerebral Blood Flow and Metabolism · doi:10.1038/jcbfm.2008.90 · Cited by 26
“For image processing, the commercial software Image-Pro Plus 4.0 (Media Cybernetics, MD, USA) was used.”
BackgroundMethodInfluentialPotential importance of B cells in aging and aging-associated neurodegenerative diseases
Biragyn, A., Aliseychik, M., & Rogaev, E. (2017) · Seminars in Immunopathology · doi:10.1007/s00281-016-0615-8 · Cited by 25
“For example, IL-4 from meningeal T cells supports memory maintenances [77] while neuronal and glia-derived TNFα regulates synaptic strength via exocytosis and endocytosis of AMPA and GABA receptors, respectively [78].”
BackgroundPersistent synaptic scaling independent of AMPA receptor subunit composition
Altimimi, H. F., & Stellwagen, D. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.1102-13.2013 · Cited by 25
“Moreover, factors that have been shown to be required for scaling up appear to target GluA1 for increased surface expression (Stellwagen et al., 2005; Stellwagen and Malenka, 2006; Aoto et al., 2008).”
BackgroundMethodSelf-citationSynaptic Dysfunction in Epilepsy
Zaitsev, A. V., Amakhin, D. V., Dyomina, A. V., Zakharova, M. V., Ergina, J. L., Postnikova, T. Y., Diespirov, G. P., & Magazanik, L. G. (2021) · Journal of Evolutionary Biochemistry and Physiology · doi:10.1134/s002209302103008x · Cited by 29
Mironets, E., Fischer, R., Bracchi-Ricard, V. C., Saltos, T. M., Truglio, T. S., O’Reilly, M. L., Swanson, K. A., Bethea, J. R., & Tom, V. J. (2019) · Journal of Neuroscience · doi:10.1523/jneurosci.2417-19.2019 · Cited by 37
“Interestingly, sTNF signaling has been associated with increasing trafficking of calcium-permeable glutamatergic receptors and decreasing levels of inhibitory GABAergic receptors at the cell membrane (Beattie et al., 2002; Stellwagen et al., 2005; Stück et al., 2012; Patel et al., 2017).”
BackgroundInfluentialHeat induced temperature dysregulation and seizures in Dravet Syndrome/GEFS+ Gabrg2 mice
Warner, T. A., Liu, Z., Macdonald, R. L., & Kang, J. (2017) · Epilepsy Research · doi:10.1016/j.eplepsyres.2017.04.020 · Cited by 25
“MARK in decreased inhibitory strength (Stellwagen et al., 2005).”
Toward a better understanding of the central consequences of intestinal inflammation
Nyuyki, K. D., & Pittman, Q. J. (2015) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12935 · Cited by 26
The Role of GluA1 in Ocular Dominance Plasticity in the Mouse Visual Cortex
Ranson, A., Sengpiel, F., & Fox, K. D. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.2078-13.2013 · Cited by 25
“Cell surface expression of GluA1 is increased by TNF and decreased by “decoy” soluble TNF receptors (Stellwagen et al., 2005), which suggests that GluA1 is the effector molecule used by a homeostatic plasticity process mediated by TNF .”
BackgroundSuchankova, P., Klang, J., Cavanna, C., Holm, G., Nilsson, S., Jönsson, E. G., & Ekman, A. (2012) · Journal of Psychiatry and Neuroscience · doi:10.1503/jpn.110024 · Cited by 27
GABA Expression and Regulation by Sensory Experience in the Developing Visual System
Miraucourt, L. S., Silva, J. S. D., Burgos, K., Li, J., Abe, H., Ruthazer, E. S., & Cline, H. T. (2012) · PLoS ONE · doi:10.1371/journal.pone.0029086 · Cited by 26
Twohig, J. P., Cuff, S. M., Yong, A. A., & Wang, E. C. Y. (2011) · Reviews in the Neurosciences · doi:10.1515/rns.2011.041 · Cited by 29
“…in neurological roles as diverse as regulating neuronal precursor development (Johansson et al., 2008 ), regulating neuronal lifespan (Yang et al., 2002b ), modulating neuronal synapse strength (Stellwagen et al., 2005 ), and directly modulating neuron excitability (Cunningham et al., 1996 ).”
BackgroundInfluentialAge-Dependent Maintenance of Motor Controland Corticostriatal Innervation by Death Receptor 3
Twohig, J. P., Roberts, M. I., Gavaldà, N., Rees-Taylor, E. L., Giralt, A., Adams, D., Brooks, S. P., Bull, M. J., Calder, C. J., Cuff, S. M., et al. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.1928-09.2010 · Cited by 23
“TNF , though, has been shown to act as a gliotransmitter, altering synaptic transmission (Stellwagen et al., 2005) and controlling synaptic strength (Beattie et al., 2002) and scaling (Stellwagen and Malenka, 2006), while other proinflammatory cytokines such as IL-1 can influence synaptic…”
BackgroundPeripheral Nerve Injury Sensitizes Neonatal Dorsal Horn Neurons to Tumor Necrosis Factor-α
Li, J., Xie, W., Zhang, J., & Baccei, M. L. (2009) · Molecular Pain · doi:10.1186/1744-8069-5-10 · Cited by 26
“Interestingly, while TNFR1 activation also decreases the exocytosis of GABAARs in hippocampal neurons [26], we observed no significant effects of TNFα on inhibitory neurotransmission in the neonatal SDH following peripheral nerve injury (Figure 2).”
BackgroundSynaptic Scaling and the Development of a Motor Network
Knogler, L. D., Liao, M., & Drapeau, P. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.0880-10.2010 · Cited by 24
Mitigation of perioperative neurocognitive disorders: A holistic approach
Safavynia, S. A., Goldstein, P. A., & Evered, L. A. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.949148 · Cited by 44
“Moreover, TNFα can cause downregulation of γ-aminobutyric acid type A (GABAA) receptors (Stellwagen et al., 2005), further shifting the balance toward excitotoxicity, hippocampal neuronal death, and cognitive impairment.”
BackgroundTaoro‐González, L., Pereda, D., Valdés‐Baizabal, C., González‐Gómez, M., Pérez, J. A., Mesa-Herrera, F., Canerina‐Amaro, A., Perez-Gonzalez, H., Rodríguez, C., Díaz, M. L., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23137430 · Cited by 26
“The tumor necrosis factor-alpha (TNF-α), another cardinal pro-inflammatory cytokine, also alters GluA1 AMPA subunit expression in both cultured hippocampal neurons and hippocampal slices [38,39].”
BackgroundCastro, M. A. D., & Volterra, A. (2021) · Glia · doi:10.1002/glia.24128 · Cited by 27
“receptors in response to reduced synaptic activity (Stellwagen et al., 2005).”
BackgroundHuang, M., Chen, M., Tu, P., Bai, Y. M., Su, T., Yang, B., Liu, R.-S., & Li, C. (2018) · Journal of Affective Disorders · doi:10.1016/j.jad.2018.04.037 · Cited by 28
Wang, W., Zinsmaier, A. K., Firestone, E., Lin, R., Yatskievych, T. A., Yang, S., Zhang, J., & Bao, S. (2018) · Journal of Neurotrauma · doi:10.1089/neu.2018.5688 · Cited by 29
“20 With regard to changes in PV + interneurons, it has been reported in a severe fluid percussion TBI model that a decrease in inhibitory synaptic transmission was paralleled by a loss of PV + interneurons in the DG 1 month after the TBI.”
Metadata
- Authors
- Stellwagen, D., Beattie, E. C., Seo, J. Y., & Malenka, R. C.
- Affiliations
- Stanford Medicine (US)
- California Pacific Medical Center (US)
- Corresponding author
- Malenka, Robert C.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-03-23
- Volume
- 25
- Issue
- 12
- Pages
- 3219-3228
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6725093
- OpenAlex
- W2134209166
- Cited by
- 985
- References
- 74
- Citations by year
- 2026: 44 · 2025: 35 · 2024: 59 · 2023: 54 · 2022: 60 · 2021: 64 · 2020: 61 · 2019: 48 · 2018: 49 · 2017: 41 · 2016: 43 · 2015: 57 · 2014: 45 · 2013: 53 · 2012: 61
- FWCI
- 11.57
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (MH63394)
- National Institute of Mental Health (F32MH065752, R37MH063394, R01MH063394, MH065752, MH63394)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- TNF-α, AMPA receptor trafficking, receptor internalization, TNFR1, phosphatidylinositol 3-kinase, excitotoxicity, hippocampal pyramidal neurons, inflammatory cytokines, synaptic homeostasis
- MeSH terms
- Animals, Animals, Newborn, Antibodies, Cells, Cultured, Dose-Response Relationship, Radiation, Drug Interactions, Electric Stimulation, Enzyme Inhibitors, Hippocampus, Immunohistochemistry, Neural Inhibition, Synaptic Transmission, Neurons, Tumor Necrosis Factor-alpha, Blotting, Western, Gene Expression, Receptors, GABA, Receptors, AMPA, Patch-Clamp Techniques, Excitatory Postsynaptic Potentials, Biotinylation, Protein Transport, Receptors, Tumor Necrosis Factor, Type I, Rats, In Vitro Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
