Neuroprotection by Glial Metabotropic Glutamate Receptors Is Mediated by Transforming Growth Factor-β

摘要: The medium collected from cultured astrocytes transiently exposed to the group-II metabotropic glutamate (mGlu) receptor agonists (2S,1′R,2′R,3′R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV) or (S)-4-carboxy-3-hydroxyphenylglycine (4C3HPG) is neuroprotective when transferred mixed cortical cultures challenged with NMDA ([Bruno et al., 1997][1]). following data indicate that this particular form of neuroprotection mediated by transforming growth factor-β (TGFβ). (1) TGFβ1 and -β2 were highly against toxicity, their action was less than additive produced treated DCG-IV 4C3HPG (GM/DCG-IV GM/4C3HPG); (2) antibodies specifically neutralized actions prevented activity 4C3HPG, as well GM/DCG-IV GM/4C3HPG; (3) a transient exposure either led delayed increase in both intracellular extracellular levels TGFβ. We therefore conclude activation mGlu receptors (presumably mGlu3 receptors) leads an increased formation release TGFβ, which turn protects neighbor neurons excitotoxic death. These results offer new strategy for increasing local production factors CNS. [1]: #ref-2