The primate-specific peptide Y-P30 regulates morphological maturation of neocortical dendritic spines

• DOI: 10.1371/journal.pone.0211151
• Publication Date: 2019-02-13T13:37:23Z
• Authors: Janine R. Neumann; Suvarna Dash-Wagh; Alexander Jack; Andrea Räk; Kay Jüngling; Mohammad I. K. Hamad; Hans-Christian Pape; Michael R. Kreutz; Martin Puskarjov; Petra Wahle
• Keywords: Filopodia; Dendritic filopodia

The 30-amino acid peptide Y-P30 corresponds to the N-terminus of primate-specific, sweat gland-derived dermcidin prepropeptide. Previous work has revealed that enhances interaction pleiotrophin and syndecans-2/3, thus represents a natural ligand study this signaling pathway. In immature neurons, activates c-Src p42/44 ERK kinase pathway, increases amount F-actin in axonal growth cones, promotes neuronal survival, cell migration elongation. action on requires syndecan-3 heparan sulfate side chains. Whether potential influence dendrites dendritic protrusions not been explored. latter is suggested by observations syndecan-2 expression during postnatal development, becomes enriched spines, overexpression neurons results premature morphological maturation spines. Here, analysing rat cortical pyramidal non-pyramidal organotypic cultures, we show does alter development arborization patterns. However, treatment decreases density apical, but basal at expense filopodia. Analysis spine morphology an unchanged mushroom/stubby-to-thin ratio shortening longest decile protrusions. Whole-cell recordings from principal dissociated cultures grown presence demonstrated decrease frequency glutamatergic mEPSCs. Despite these differences protrusion synaptic transmission, likely attributable presynaptic effects, calcium event rate amplitude recorded were altered treatment. Together, our data suggest capacity decelerate spinogenesis promote morphological, synaptic,