Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation.
Francesca Romana RizzoAlessandra MusellaFrancesca De VitoDiego FresegnaSilvia BullittaValentina VanniLivia GuadalupiMario Stampanoni BassiFabio ButtariGeorgia MandolesiDiego CentonzeAntonietta GentilePublished in: Neural plasticity (2018)
Cytokines are constitutively released in the healthy brain by resident myeloid cells to keep proper synaptic plasticity, either in the form of Hebbian synaptic plasticity or of homeostatic plasticity. However, when cytokines dramatically increase, establishing a status of neuroinflammation, the synaptic action of such molecules remarkably interferes with brain circuits of learning and cognition and contributes to excitotoxicity and neurodegeneration. Among others, interleukin-1β (IL-1β) and tumor necrosis factor (TNF) are the best studied proinflammatory cytokines in both physiological and pathological conditions and have been invariably associated with long-term potentiation (LTP) (Hebbian synaptic plasticity) and synaptic scaling (homeostatic plasticity), respectively. Multiple sclerosis (MS) is the prototypical neuroinflammatory disease, in which inflammation triggers excitotoxic mechanisms contributing to neurodegeneration. IL-β and TNF are increased in the brain of MS patients and contribute to induce the changes in synaptic plasticity occurring in MS patients and its animal model, the experimental autoimmune encephalomyelitis (EAE). This review will introduce and discuss current evidence of the role of IL-1β and TNF in the regulation of synaptic strength at both physiological and pathological levels, in particular speculating on their involvement in the synaptic plasticity changes observed in the EAE brain.
Keyphrases
- multiple sclerosis
- white matter
- rheumatoid arthritis
- end stage renal disease
- resting state
- mass spectrometry
- ejection fraction
- newly diagnosed
- cerebral ischemia
- traumatic brain injury
- oxidative stress
- prognostic factors
- induced apoptosis
- lipopolysaccharide induced
- patient safety
- bone marrow
- signaling pathway
- acute myeloid leukemia
- brain injury
- cell proliferation
- pi k akt
- patient reported