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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.
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“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
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“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
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Cites
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“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
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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).”
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“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
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“…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).”
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“…have found TNF-α induced membrane insertion of new AMPA receptors to be phosphatidylinositol 3 kinase (PI3K) dependent (Leonoudakis et al., 2008; Stellwagen et al., 2005) and have reported that phosphorylation of the GluA1 AMPA subunit at serine 845 by protein kinase A promotes receptor…”
BackgroundInfluentialGlial Tumor Necrosis Factor Alpha (TNFα) Generates Metaplastic Inhibition of Spinal Learning
Huie, J. R., Baumbauer, K. M., Lee, K. H., Bresnahan, J. C., Beattie, M. S., Ferguson, A. R., & Grau, J. W. (2012) · PLoS ONE · doi:10.1371/journal.pone.0039751 · Cited by 53
“Previous research has shown that neuronal TNFa receptor activation causes an increase in membrane trafficking of GluR2-lacking AMPA receptors [39].”
BackgroundDahlin, M. G., Singleton, S. S., David, J. A., Basuchoudhary, A., Wickström, R., Mazumder, R., & Prast‐Nielsen, S. (2022) · EBioMedicine · doi:10.1016/j.ebiom.2022.104061 · Cited by 69
Alzheimer’s Disease: Exploring the Role of Inflammation and Implications for Treatment
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“Elevated levels of TNF alpha cause a rapid increase in excitatory synaptic strength and weakening in inhibitory synaptic strength [58, 59].”
Growth factors in synaptic function
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“Tumor necrosis factor (TNFα) can mediate synaptic plasticity and strength during development, as well as receptor trafficking that impacts excitatory and inhibitory synapses [7, 63, 64].”
BackgroundMolecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants
Pathak, D., & Sriram, K. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24032272 · Cited by 72
Karimi-Haghighi, S., Dargahi, L., & Haghparast, A. (2020) · Addiction Biology · doi:10.1111/adb.12740 · Cited by 56
Alexithymia in multiple sclerosis: A systematic review of literature
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“The inflammatory mediators can result in a neurochemical imbalance, mainly an upregulation of the excitatory glutamatergic transmission (Stellwagen et al., 2005; Lai et al., 2006; Mizuno et al., 2008), and a down regulation of the inhibitory GABAergic transmission (Stellwagen et al.”
BackgroundEpilepsy-associated alterations in hippocampal excitability
Navidhamidi, M., Ghasemi, M., & Mehranfard, N. (2017) · Reviews in the Neurosciences · doi:10.1515/revneuro-2016-0059 · Cited by 61
An integrated cytokine and kynurenine network as the basis of neuroimmune communication
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“- Regulates GABA transmission and anxiety (T59) - Determines inflammatory status in MS, ALS (T44, T60) - Regulates myelination stability and inflammation (T61) - Upregulated by atypical antispsychotics (T62, T63) IL-15 - Increased and released by local inflammation (T64, T65) - Promotes neurogenesis and maintains syna…”
BackgroundInfluentialDoes Traumatic Brain Injury Cause Risky Substance Use or Substance Use Disorder?
Olsen, C. M., & Corrigan, J. D. (2021) · Biological Psychiatry · doi:10.1016/j.biopsych.2021.07.013 · Cited by 66
Madsen, P. M., Clausen, B. H., Degn, M., Thyssen, S., Kristensen, L. K., Svensson, M., Ditzel, N., Finsen, B. R., Deierborg, T., Brambilla, R., et al. (2015) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x15610339 · Cited by 59
“Though alterations in these functions in TNF / mice were often ascribed to abnormal serotonine metabolism(69) or changes in nerve growth factor levels,(59) they are likely also associated with the important role of glial-derived TNF in homeostatic activity-dependent regulation of synaptic connectivity(13) and control…”
BackgroundCrawford, D. C., Jiang, X., Taylor, A., & Mennerick, S. J. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.2604-12.2012 · Cited by 57
“In contrast, TNF (1 ng/ml), an astrocyte-derived factor involved in postsynaptic plasticity (Beattie et al., 2002; Stellwagen et al., 2005; Stellwagen and Malenka, 2006; Steinmetz and Turrigiano, 2010), did not rescue muting in astrocyte-poor cultures (Fig.”
BackgroundTsui, J., & Malenka, R. C. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m600966200 · Cited by 51
Self-citationMing, Z., Sawicki, G., & Bekar, L. (2015) · Neuroscience Letters · doi:10.1016/j.neulet.2015.01.081 · Cited by 54
The Role of Inflammation in Tinnitus: A Systematic Review and Meta-Analysis
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“TNF-α expression influences inhibitory GABAA (gamma-aminobutyric acid) receptors by causing an endocytosis of GABAA receptors, resulting in fewer surface GABAA receptors and a decrease in inhibitory synaptic strength [72].”
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Role of astrocytes in synapse formation and maturation
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Pleiotropic actions of allopregnanolone underlie therapeutic benefits in stress-related disease
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Inflammatory Processes, Febrile Seizures, and Subsequent Epileptogenesis
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“TNF-α has been found to increase surface expression of AMPA receptors and decreasing GABA receptors (89), thus leading to long-term changes in neuronal excitability (90).”
BackgroundFacilitation of AMPA Receptor Synaptic Delivery as a Molecular Mechanism for Cognitive Enhancement
Knafo, S., Venero, C., Sánchez‐Puelles, C., Pereda-Pérez, I., Franco, A. C. G., Sandi, C., Suárez, L. M., Solís, J. M., Alonso‐Nanclares, L., Martín, E. D., et al. (2012) · PLoS Biology · doi:10.1371/journal.pbio.1001262 · Cited by 313
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BackgroundStrain Dependent Effects of Prenatal Stress on Gene Expression in the Rat Hippocampus
Neeley, E. W., Berger, R., Koenig, J., & Leonard, S. (2011) · Physiology and Behavior · doi:10.1016/j.physbeh.2011.02.032 · Cited by 52
“The cytokine can up-regulate AMPA receptors and simultaneously decrease synaptic inhibition through endocytosis of GABA receptors [57].”
Synaptic P2X7 Receptor Regenerative-Loop Hypothesis for Depression
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Costagliola, G., Depietri, G., Michev, A., Riva, A., Foiadelli, T., Savasta, S., Bonuccelli, A., Peroni, D. G., Consolini, R., Marseglia, G. L., et al. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.741244 · Cited by 56
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BackgroundNamba, M. D., Kupchik, Y. M., Spencer, S. M., García‐Keller, C., Goenaga, J. G., Powell, G. L., Vicino, I., Hogue, I. B., & Gipson, C. D. (2019) · Addiction Biology · doi:10.1111/adb.12797 · Cited by 59
“TNFα both increases surface expression of calcium permeable AMPA receptors and decreases surface expression of GABAA receptors within hippocampal slices, resulting in significant increases in excitatory synaptic strength (Stellwagen et al., 2005).”
BackgroundResultInfluentialBrain tumor necrosis factor-α mediates anxiety-like behavior in a mouse model of severe obesity
Fourrier, C., Bosch‐Bouju, C., Boursereau, R., Sauvant, J., Aubert, A., Capuron, L., Ferreira, G., Layé, S., & Castanon, N. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.11.316 · Cited by 55
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Hook, M., Washburn, S., Moreno, G. L., Woller, S., Puga, D., Lee, K. H., & Grau, J. (2010) · Brain, behavior, and immunity · doi:10.1016/j.bbi.2010.10.018 · Cited by 51
“…increase tyrosine phosphorylation of the NMDA receptor NR2B subunit (Viviani et al., 2003), increase surface expression of AMPA receptors (Stellwagen et al., 2005), and has been linked to inhibition of glutamate transporters such as GLT-1 and GLAST (Tai et al., 2006; Prow and Irani,…”
Microglial Responses to Stress-Induced Depression: Causes and Consequences
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BackgroundBidirectional homeostatic plasticity induced by interneuron cell death and transplantation in vivo
Howard, M. A., Rubenstein, J. L. R., & Baraban, S. C. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1307784111 · Cited by 56
“Although homeostatic synaptic plasticity has been studied extensively in vitro (15, 40, 41), little is known about the role it plays in neurological abnormalities such as interneuronopathy.”
BackgroundPeripheral Interleukin‐1β Levels are Elevated in Chronic Tension‐Type Headache Patients
Vedova, C. B. D., Cathcart, S., Dohnalek, A., Lee, V., Hutchinson, M. R., Immink, M. A., & Hayball, J. D. (2013) · Pain Research and Management · doi:10.1155/2013/796161 · Cited by 50
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Ferguson, A. R., Bolding, K. A., Huie, J. R., Hook, M. A., Santillano, D. R., Miranda, R. C., & Grau, J. W. (2008) · Journal of Neuroscience · doi:10.1523/jneurosci.3098-08.2008 · Cited by 48
Taoro‐González, L., Arenas, Y. M., Cabrera‐Pastor, A., & Felipo, V. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1082-z · Cited by 48
“TNF-α selectively enhances membrane expression of GluA1 in hippocampal neurons and the proportion of GluA2-lacking receptors, resulting in AMPA receptors with different properties becoming calcium-permeable, inwardly rectifying and inhibited by polyamines [61].”
Hennekinne, L., Colasse, S., Triller, A., & Renner, M. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.5247-12.2013 · Cited by 48
“TNF affects the balance between excitatory and inhibitory synaptic transmission in the hippocampus by increasing the insertion of GluA1-containing AMPARs and reducing the surface amount of GABA receptors (Stellwagen et al., 2005; Beattie et al., 2010).”
BackgroundMethodRen, S., Breuillaud, L., Yao, W., Yin, T., Norris, K. A., Zehntner, S. P., & D’Adamio, L. (2021) · Journal of Biological Chemistry · doi:10.1074/jbc.ra120.016395 · Cited by 47
“In addition to boosting excitatory transmission, TNF-α decreases inhibitory synaptic strength by promoting endocytosis of γ-aminobutyric acid (GABA) receptors, hence reducing surface GABA receptors (10).”
BackgroundNeuropathophysiological Mechanisms and Treatment Strategies for Post-traumatic Epilepsy
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“We have previously reported that chronic morphine administration increases PAG cytokine expression (IL-1β, IL-6 and TNF) in males and that this local neuroinflammatory response actively opposes the analgesic effects of morphine [24].”
BackgroundMing, Z., Wotton, C. A., Appleton, R. T., Ching, J. C. H., Loewen, M. E., Sawicki, G., & Bekar, L. K. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0259-y · Cited by 49
“Likewise, TNF-α, implicated in plasticity and synaptic scaling [15,16], can also decrease the inhibition/excitation ratio via increasing glutamate AMPA receptor insertion and GABAA receptor internalization in central synapses [17].”
BackgroundResultEvidence of tumor necrosis factor receptor 1 signaling in human temporal lobe epilepsy.
Yamamoto, A., Schindler, C., Murphy, B., Bellver-Estellés, C., So, N., Taki, W., Meller, R., Simon, R., & Henshall, D. (2006) · Experimental Neurology · doi:10.1016/j.expneurol.2006.07.003 · Cited by 47
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Clark, S. M., Notarangelo, F. M., Li, X., Chen, S., Schwarcz, R. M., & Tonelli, L. H. (2018) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2018.09.011 · Cited by 50
Tumour necrosis factor - alpha mediated mechanisms of cognitive dysfunction
Baune, B. T., Camara, M.-L., Eyre, H. A., Jawahar, M. C., Anscomb, H., & Körner, H. (2012) · Translational Neuroscience · doi:10.2478/s13380-012-0027-8 · Cited by 50
“Furthermore TNF-α increases amplitude of miniature excitatory postsynaptic currents (mEPSC) and decreases miniature inhibitory postsynaptic currents (mIPSC) [32,84].”
InfluentialZhao, P., Leonoudakis, D., Abood, M. E., & Beattie, E. C. (2009) · Neuropharmacology · doi:10.1016/j.neuropharm.2009.07.035 · Cited by 44
“We previously characterized TNFa as a powerful glial-derived instigator of AMPAR trafficking to the plasma membrane (Beattie et al., 2002; Stellwagen et al., 2005).”
BackgroundMethodInfluentialSelf-citationTNF-α involves in altered prefrontal synaptic transmission in mice with persistent inflammatory pain
Jia, D., Gao, G., Liu, Y., He, S., Zhang, X., Zhang, Y., & Zhao, M. (2006) · Neuroscience Letters · doi:10.1016/j.neulet.2006.12.032 · Cited by 44
The Role of Pro-inflammatory Cytokines in Memory Processes and Neural Plasticity
Goshen, I., & Yirmiya, R. (2007) · Elsevier eBooks · doi:10.1016/b978-012088576-3/50021-6 · Cited by 47
Medalla, M., Chang, W., Calderazzo, S. M., Go, V., Tsolias, A., Goodliffe, J. W., Pathak, D., de Alba, D., Pessina, M. A., Rosene, D. L., et al. (2020) · Journal of Neuroscience · doi:10.1523/jneurosci.2226-19.2020 · Cited by 51
“Glialderived TNF-a can promote GABAA receptor endocytosis and AMPA receptor exocytosis (Stellwagen et al., 2005; review Leidenheimer, 2008).”
BackgroundShim, H. G., Jang, S.-S., Kim, S. H., Hwang, E. M., Min, J. O., Kim, H. Y., Kim, Y. S., Ryu, C., Chung, G., Kim, Y., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-29786-9 · Cited by 49
Cabrera‐Pastor, A., Hernández‐Rabaza, V., Taoro‐González, L., Balzano, T., Llansola, M., & Felipo, V. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.05.011 · Cited by 43
“In contrast, IL-1b increased membrane expression of GluA1 more slightly (Stellwagen et al, 2005) or, at high concentrations, reduces it (Lai et al, 2006).”
Pilat, D., Rojewska, E., Jurga, A., Piotrowska, A., Makuch, W., Przewłocka, B., & Mika, J. (2015) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2015.05.058 · Cited by 45
“, 2003), and increase surface expression of AMPA receptors (Stellwagen et al., 2005).”
BackgroundCytokines and neuronal channels: A molecular basis for age-related decline of neuronal function?
Viviani, B., & Boraso, M. (2010) · Experimental Gerontology · doi:10.1016/j.exger.2010.09.008 · Cited by 46
The brain cytokine orchestra in multiple sclerosis: from neuroinflammation to synaptopathology
Amoriello, R., Memo, C., Ballerini, L., & Ballerini, C. (2024) · Molecular Brain · doi:10.1186/s13041-024-01077-7 · Cited by 47
“Similar CKs effects are also implicated in the excitotoxic phenomena that characterize amyotrophic lateral sclerosis pathogenesis, where motoneurons are more vulnerable to glutamate-induced cell death [26, 33–36].”
BackgroundA Rationale for Allopregnanolone Treatment of Alcohol Use Disorders: Basic and Clinical Studies
Morrow, A. L., Boero, G., & Porcu, P. (2019) · Alcoholism Clinical and Experimental Research · doi:10.1111/acer.14253 · Cited by 53
“…signaling via the classic pro-inflammatory cytokines in brain appears to enhance glutamatergic transmission and reduce GABAergic transmission (Stellwagen et al., 2005, Pribiag and Stellwagen, 2013, Ferguson et al., 2008, Stuck et al., 2012) rather than produce other signs of inflammation…”
BackgroundInteractions of Opioids and HIV Infection in the Pathogenesis of Chronic Pain
Liu, B., Liu, X., & Tang, S. (2016) · Frontiers in Microbiology · doi:10.3389/fmicb.2016.00103 · Cited by 43
“Tat or gp120 can evoke an increase in intracellular Ca2+ ([Ca2+]i) in astroglia (Haughey et al., 1999; Holden et al., 1999).”
BackgroundInfluentialWang, X., Lippi, G., Carlson, D. M., & Berg, D. K. (2013) · Journal of Neurochemistry · doi:10.1111/jnc.12436 · Cited by 43
Mechanisms of Plasticity in the Developing and Adult Visual Cortex
Sur, M., Nagakura, I., Chen, N., & 杉原, 弘. (2013) · Progress in brain research · doi:10.1016/b978-0-444-63327-9.00002-3 · Cited by 44
An emerging role for microglia in stress‐effects on memory
Sanguino‐Gómez, J., Buurstede, J. C., Abiega, O., Fitzsimons, C. P., Lucassen, P. J., Eggen, B. J. L., Lesuis, S. L., Meijer, O. C., & Krugers, H. J. (2021) · European Journal of Neuroscience · doi:10.1111/ejn.15188 · Cited by 43
Glial neuroimmune signaling in opioid reward
Zhang, H., Largent‐Milnes, T. M., & Vanderah, T. W. (2019) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2019.11.012 · Cited by 50
Lecca, D., Bader, M., Tweedie, D., Hoffman, A. F., Jung, Y. J., Hsueh, S., Hoffer, B. J., Becker, R. E., Pick, C. G., Lupica, C. R., et al. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104528 · Cited by 45
“Through these mechanisms, heightened TNF-α changes the balance between synaptic excitation and inhibition (Stellwagen et al., 2005; Ogoshi et al., 2005) and, consequent to excessive Ca input into neurons, can induce neuronal cell dysfunction and death.”
BackgroundLi, J., Xu, B., Chen, Z., Zhou, C., Liao, L., Qin, Y., Yang, C., Zhang, X., Hu, Z., Sun, L., et al. (2018) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/1440-1681.12918 · Cited by 46
Role of neuroinflammation in morphine tolerance: Effect of tumor necrosis factor-α
Shen, C., Tsai, R.-Y., & Wong, C. (2012) · Acta anaesthesiologica Taiwanica · doi:10.1016/j.aat.2012.12.004 · Cited by 39
Batti, L., & O'Connor, J. J. (2009) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2009.11.002 · Cited by 37
“, 1992) and interfere with alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) and gamma-aminobutyric acid (GABAR) recycling (Stellwagen et al., 2005).”
BackgroundHermann, G. E., & Rogers, R. C. (2009) · Brain Research · doi:10.1016/j.brainres.2009.03.059 · Cited by 43
“We have shown that TNF activates vagal afferent terminals (Rogers et al., 2006) [which are predominantly glutamatergic] and, in other brain areas, TNF immediately upregulates AMPA receptor function post synaptically (Pickering et al., 2005; Stellwagen et al., 2005).”
BackgroundMalaguarnera, M., Llansola, M., Balzano, T., Gómez-Giménez, B., Antúnez-Muñoz, C., Martínez-Alarcón, N., Mahdinia, R., & Felipo, V. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.00132 · Cited by 42
“Different pro-inflammatory cytokines, such as TNFα, IL1β and IL-6, modulate GABAA receptor function in an area- and dose-dependent manner (Stellwagen et al., 2005; García-Oscos et al., 2012; Pribiag and Stellwagen, 2013).”
BackgroundLi, T., Zhai, X., Jiang, J., Song, X., Han, W., Ma, J., Xie, L., Li, C., Chen, H., & Jiang, L. (2016) · Brain Research · doi:10.1016/j.brainres.2016.12.006 · Cited by 40
Inflammation and neurodegenerative disorders
Baune, B. T. (2015) · Current Opinion in Psychiatry · doi:10.1097/yco.0000000000000140 · Cited by 49
“In addition, the role TNF-a plays in LTP and long-term depression formation by upregulation of a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors [93] and endocytosis of gamma-aminobutyric acid receptors [94] is crucial in the development of synaptic neuroplasticityrelated memory and learning [95].”
BackgroundBennett, D. A., & Brookoff, D. (2006) · doi:10.1111/j.1526-4637.2006.00124.x · Cited by 42
Pattern recognition receptors in chronic pain: Mechanisms and therapeutic implications
Kato, J., Agalave, N. M., & Svensson, C. I. (2016) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2016.06.039 · Cited by 44
Little cells of the little brain: microglia in cerebellar development and function
Stoessel, M. B., & Majewska, A. K. (2021) · Trends in Neurosciences · doi:10.1016/j.tins.2021.04.001 · Cited by 49
Tumor Necrosis Factor Alpha in Amyotrophic Lateral Sclerosis: Friend or Foe?
Guidotti, G., Scarlata, C., Brambilla, L., & Rossi, D. (2021) · Cells · doi:10.3390/cells10030518 · Cited by 42
Chen, S., Zeng, X., Zong, W., Wang, X., Chen, L., Zhou, L., Li, C., Huang, Q., Huang, X., Zeng, G., et al. (2019) · Neurochemical Research · doi:10.1007/s11064-018-2700-y · Cited by 48
Rossi, S., Motta, C., Musella, A., & Centonze, D. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.09.022 · Cited by 42
Carriba, P., Jiménez, S., Navarro, V., Moreno‐González, I., Barneda‐Zahonero, B., Moubarak, R. S., López‐Soriano, J., Gutiérrez, A., Vitórica, J., & Comella, J. X. (2015) · Cell Death and Disease · doi:10.1038/cddis.2015.6 · Cited by 40
Kintz, N. M., Petzinger, G. M., Akopian, G. K., Ptasnik, S., Williams, C., Jakowec, M. W., & Walsh, J. P. (2013) · Journal of Neuroscience Research · doi:10.1002/jnr.23260 · Cited by 39
“In support of our approach, others have demonstrated that changes in cell surface expression of AMPARs may contribute to and thus provide insight into changes in synaptic receptor expression (Stellwagen et al., 2005; Kessels et al., 2009; Tao-Cheng et al., 2011).”
ResultTurovskaya, M. V., Turovsky, E. A., Зинченко, В. П., Levin, S. G., & Godukhin, O. V. (2012) · Neuroscience Letters · doi:10.1016/j.neulet.2012.03.084 · Cited by 40
Kwon, M., Lee, J.-K., Park, S.-H., Sim, Y., Jung, J., Won, M., Kim, S., & Suh, H. (2010) · Korean Journal of Physiology and Pharmacology · doi:10.4196/kjpp.2010.14.5.257 · Cited by 34
“Recently, it has been demonstrated that proinflammatory cytokines have established potent pro-excitatory actions [28-31].”
BackgroundBellizzi, M. J., Lu, S., & Gelbard, H. A. (2006) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-005-9006-y · Cited by 37
“…on which receptor types it activates (Perry et al. 2002; Bernardino et al. 2005), likely augments AMPA receptor-mediated glutamate toxicity in neurons (Gelbard et al. 1993; Hermann et al. 2001) by increasing the membrane expression of Ca2+-permeable AMPA receptors (Stellwagen et al. 2005).”
BackgroundStone, T. W., & Williams, R. O. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.16015 · Cited by 45
The complex role of inflammation and gliotransmitters in Parkinson's disease
Gopinath, A., Mackie, P. M., Phan, L. T., Tansey, M. G., & Khoshbouei, H. (2022) · Neurobiology of Disease · doi:10.1016/j.nbd.2022.105940 · Cited by 48
Immunity, Ion Channels and Epilepsy
Chen, T., Lai, M., Huang, H.-Y. I., Wu, S., & Huang, C. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23126446 · Cited by 46
“fl , , fl i ti t f r l t ( ‐ ‐ ‐ ‐ ‐ ‐ ‐ , ‐ Υ‐aminobutyric acid (GABAA) receptors and altering their receptor subunits [31].”
BackgroundInfluentialZhang, W., Xiong, B., Zhang, L., Huang, X., Zhou, W., Zou, Q., Manyande, A., Wang, J., Tian, X., & Tian, Y. (2020) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.13388 · Cited by 42
“At the same time, the levels of surface α5GABAARs were up-regulated in the laparotomy mice (F(2,12) = 6.”
BackgroundLazić, D., Tešić, V., Jovanović, M., Brkić, M., Milanović, D., Zloković, B. V., Kanazir, S., & Perović, M. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.104745 · Cited by 40
“…and Al-Ayadhi, 2014), as TNFα induces a rapid and persistent decrease of inhibitory synaptic strength (Pribiag and Stellwagen, 2013), and thus, regulates neuronal circuit homeostasis in a manner that may exacerbate excitotoxic damage resulting from neuronal insults (Stellwagen et al., 2005).”
BackgroundMironets, E., Osei‐Owusu, P., Bracchi-Ricard, V. C., Fischer, R., Owens, E. A., Ricard, J., Wu, D., Saltos, T. M., Collyer, E., Hou, S., et al. (2018) · Journal of Neuroscience · doi:10.1523/jneurosci.2376-17.2018 · Cited by 60
“Intriguingly, increased TNF is associated with various forms of plasticity that can increase neuronal excitability (Beattie et al., 2002; Stellwagen et al., 2005; Stück et al., 2012).”
BackgroundInfluentialTumor Necrosis Factor Potentiates Central Vagal Afferent Signaling by Modulating Ryanodine Channels
Rogers, R. C., Meter, M. J. V., & Hermann, G. E. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.3530-06.2006 · Cited by 37
“Although the connection between TNF receptor activation and the rapid regulation of CD38 is not presently clear, convincing evidence suggests that TNF can potently affect neurotransmission through rapid control of receptor trafficking (Stellwagen et al., 2005).”
BackgroundInfluentialMore than a sidekick: glia and homeostatic synaptic plasticity
Turrigiano, G. G. (2006) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2006.08.002 · Cited by 39
Landi, D., Vollaro, S., Pellegrino, G., Mulas, D., Ghazaryan, A., Falato, E., Pasqualetti, P., Rossini, P. M., & Filippi, M. (2014) · Clinical Neurophysiology · doi:10.1016/j.clinph.2014.05.031 · Cited by 43
“…as TNFalpha, IL-1 (Noda et al., 2013) and IFNgamma (Serpero et al., 2013), which are able to induce hyperactivity of glutamatergic transmission (Stellwagen et al., 2005; Lai et al., 2006; Stellwagen and Malenka, 2006; Mizuno et al., 2008; Centonze et al., 2009a); it also modifies the behavior…”
BackgroundMicroglia modulate TNFα ‐mediated synaptic plasticity
Kleidonas, D., Kirsch, M., Andrieux, G., Pfeifer, D., Boerries, M., & Vlachos, A. (2023) · Glia · doi:10.1002/glia.24383 · Cited by 37
Huang, R., Gao, Y., Chen, J., Duan, Q., He, P., Zhang, J., Huang, H., Zhang, Q., Ma, G., Zhang, Y., et al. (2022) · Neuroscience · doi:10.1016/j.neuroscience.2022.02.028 · Cited by 41
Hyperacute Excitotoxic Mechanisms and Synaptic Dysfunction Involved in Traumatic Brain Injury
Hoffe, B., & Holahan, M. R. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.831825 · Cited by 43
“Another mechanism includes the TNF-α induced increase in AMPAr lacking GluR2, increasing the Ca2+ permeability (Stellwagen et al., 2005; for review see Olmos and Lladó, 2014).”
BackgroundMedical treatment of Rasmussen's Encephalitis: A systematic review
Lagarde, S., Boucraut, J., & Bartoloméi, F. (2022) · Revue Neurologique · doi:10.1016/j.neurol.2022.01.007 · Cited by 46
Dong, R., Huang, R., Shi, X., Xu, Z., & Mang, J. (2021) · Bioengineered · doi:10.1080/21655979.2021.2006966 · Cited by 48
“ILs can also enhance the expression of MMPs, resulting in increased vascular permeability [71,72].”
BackgroundAmyotrophic Lateral Sclerosis, a Multisystem Pathology: Insights into the Role of TNF α
Tortarolo, M., Coco, D. L., Veglianese, P., Vallarola, A., Giordana, M. T., Marcon, G., Beghi, E., Poloni, M., Strong, M. J., Iyer, A. M., et al. (2017) · Mediators of Inflammation · doi:10.1155/2017/2985051 · Cited by 43
“Finally, besides increasing the surface expression of glutamate receptors, TNFα also induces endocytosis of GABA-A receptors, reducing their inhibitory action [128].”
BackgroundBertoglio, D., Verhaeghe, J. A. J., Santermans, E., Amhaoul, H., Jonckers, E., Wyffels, L., der Linden, A. V., Hens, N., Staelens, S. G., & Dedeurwaerdere, S. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.12.015 · Cited by 36
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
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