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Df(16)A+/? mice show impaired formation of dendrites and spines in the HPC ( Mukai et?al., 2008) and the PFC ( Figures S6A�CS6C), which are faithfully recapitulated in primary neuronal cultures. Impairment in these processes in Df(16)A+/? mice could only be partially accounted for by Androgen Receptor Antagonist nmr the 50% decrease in the levels of Dgcr8 ( F��nelon et?al., 2011; Stark et?al., 2008). Localization of Mirta22 within the Golgi apparatus and dendritic shafts suggests that diminishment of the miR-185 repression on Mirta22 levels may also contribute to these deficits. To test this hypothesis, we first asked whether reduction of miR-185 levels results in deficits in dendritic and spine development similar to those observed in Df(16)A+/? neurons ( Mukai et?al., 2008). We introduced an anti-miR-185 and a scramble control LNA oligo into WT primary hippocampal neurons and measured dendritic and spine morphology 2?days posttransfection at DIV9 and DIV19, respectively. Analysis of dendritic architecture indicated that reduction of miR-185 levels leads to deficits in dendritic complexity ( Figure?6A), including a significant reduction in the number of primary dendrites (21%, p?Selleckchem Roxadustat reduction in their median width (15% decrease, p?Adenylate cyclase ( Mukai et?al., 2008). We transfected primary?hippocampal neurons from Df(16)A+/? mice and their WT littermates with pre-mir-185 or prescramble. A cotransfected GFP reporter plasmid allowed us to analyze the dendritic architecture ( Figures 6G�C6I) and spine morphology ( Figures 6J�C6L) of pyramidal neurons 2?days posttransfection at DIV9 and DIV19, respectively. Consistent with previous results ( Mukai et?al., 2008), compared to WT neurons, Df(16)A+/? neurons transfected with prescramble showed reduced dendritic complexity as manifested by a decrease in the number of primary dendrites (25%, p?