Cheng B, Christakos S, Mattson MP.
Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis, Neuron 12(1) :139-53, 1994.
Abstract
Emerging data indicate that neurotrophic factors and cytokines utilize similar signal transduction mechanisms. Although neurotrophic factors
can protect CNS neurons against a variety of insults, the role of cytokines in the injury response is unclear. We now report that TNF beta
and TNF alpha (1-100 ng/ml) can protect cultured embryonic rat hippocampal, septal, and cortical neurons against glucose
deprivation-induced injury and excitatory amino acid toxicity. The elevation of intracellular calcium concentration ([Ca2+]i) induced by
glucose deprivation, glutamate, NMDA, or AMPA was attenuated in neurons pretreated with TNF beta. The mechanism whereby TNFs stabilize [Ca2+]i may involve regulation of the expression of proteins involved in maintaining [Ca2+]i homeostasis, since both TNF beta and
TNF alpha caused a 4- to 8-fold increase in the number of neurons expressing the calcium-binding protein calbindin-D28k. These data suggest a neuroprotective role for TNFs in the brain's response to injury.
Important Points:
-Model: rat culture
-TNF-a (1-100 ng/ml) and B increase the expression of calcium-binding protein positive neurons
-this protects from neurotoxicity and other forms of trauma
-TNF also affects cell membrane permeability, and neuron/glial potassium and calcium channels, among other molecular effects
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