Adrenomedullin restores the human cortical interneurons migration defects induced by hypoxia

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Abstract
Extremely preterm birth (at ADM ) as the gene with the highest fold change increase in expression. Based on previous literature about the protective role of supplemental ADM for other injuries, here, we demonstrated that addition of exogenous ADM to the hypoxic media restores the migration defects of interneurons. Lastly, we showed that one of the mechanisms of protection by ADM is through the activation of the cAMP/PKA pathway and subsequent pCREB-dependent rescued expression of a subset of GABA receptors, which are known to promote migration. Overall, in this manuscript, we provide the first direct evidence for hypoxia-induced deficits in the migration of human cortical interneurons and identify ADM as a possible target for therapeutic development.
Funding Information
  • Knut och Alice Wallenbergs Stiftelse
  • Stanford Maternal and Child Health Research Institute
  • Vetenskapsrådet
  • Gates Foundation

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