What resolves this contention: Different upstream regulators converge on VIP-IN dysfunction (MeCP2 in Rett vs TCF4 in psychiatric risk), with different reported effects (cell-autonomous activity changes vs density and connectivity changes). Whether all converge on a shared VIP cellular phenotype or on distinct mechanisms is unresolved. / In addition, ~80% of VIP interneurons expressed MeCP2, suggesting a previously unappreciated potential role for this signaling pathway in VIP interneuron development and function. / Psychiatric risk gene Transcription Factor 4 (TCF4) regulates the density and connectivity of cortical interneurons.
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