Reciprocal actions of interleukin‐6 and brain‐derived neurotrophic factor on rat and mouse primary sensory neurons
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abstract
AbstractIn low‐density, serum‐free cultures of neurons from embryonic rat dorsal root ganglia, interleukin‐6 supports the survival of less than one third of the neurons yet virtually all of them bear interleukin‐6 α‐receptors. A finding that might explain this selectivity is that interleukin‐6 acts on sensory neurons in culture through a mechanism requiring endogenous brain‐derived neurotrophic factor. Antibodies or a trkB fusion protein that block the biological activity of brain‐derived neurotrophic factor synthesized by dorsal root ganglion neurons also block the survival‐promoting actions of interleukin‐6 on these neurons. Two results indicate that interleukin‐6 influences synthesis of brain‐derived neurotrophic factor in adult dorsal root ganglion neurons. Intrathecal infusion of interleukin‐6 in rats increases the concentration of brain‐derived neurotrophic factor mRNA in rat lumbar dorsal root ganglia. The induction of brain‐derived neurotrophic factor in dorsal root ganglion neurons that is seen after nerve injury in rats or wild‐type mice is severely attenuated in mice with null mutation of the interleukin‐6 gene. In brief, the ability of interleukin‐6 to support the survival of embryonic sensory neurons in vitro depends upon the presence of endogenous brain‐derived neurotrophic factor and the induction of brain‐derived neurotrophic factor in injured adult sensory neurons depends upon the presence of endogenous interleukin‐6.
