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Microglia/motor neuron interactions in response to ATP and BDNF
Author(s) -
Watters Jyoti J,
Mitchell Gordon S,
Richards Victoria E
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.607.5
Subject(s) - microglia , neuroscience , motor neuron , neuron , synapse , biology , cell , tropomyosin receptor kinase b , microbiology and biotechnology , neurotrophic factors , receptor , inflammation , immunology , spinal cord , biochemistry
Microglia are CNS resident immune cells that remove cellular debris during normal brain development and synaptic remodeling. Their ability to sense and respond to neuronal signals is critical for maintaining a healthy CNS. Microglial activities are also important in disease, including motor neuron diseases such as ALS as well as spinal injury. However, interactions between microglia and motor neurons are not well understood. Two regulators of microglial and motor neuron function are ATP and BDNF; BDNF plays a central role in neuroplasticity, and ATP potently regulates microglial immune functions. We hypothesized that cell/cell interactions between microglia and motor neurons modulate their respective responses to BDNF and ATP. To test this hypothesis, a transwell system was used wherein motor neuron‐like NSC‐34 cells and N9 microglia were cultured alone or together in transwells without physical contact. BDNF and ATP synergistically promoted ERK activation within 2 hrs in microglia (not motor neurons) in the transwells, but not when cultured alone. ATP also increased TrkB receptor expression in both cell types 24 hrs following exposure, but only when cultured in transwells. Although the soluble molecule(s) mediating this communication are not yet clear, cell/cell interactions appear to be important for amplifying cellular responses to ATP and BDNF. Supported by NIH NS040933 and T32 HL007654 (VER).