MiRNAs regulate gene expression post-transcriptionally by causing translational repression or mRNA degradation. Mature miRNAs are incorporated into RNP complexes, miRNPs, which are responsible for silencing of mRNA targets, but mechanistic details of how miRNPs repress protein synthesis are still poorly understood. We study the mechanism of the miRNA repression in HeLa and hepatoma cells, using mRNAs whose translation is inhibited by let-7 or miR-122, the latter miRNA being specifically expressed in liver. Studies with reporter and endogenous mRNAs (e.g. mRNA encoding the cationic amino acid transporter (CAT-1) indicated that miRNAs repress translation at the initiation step and that repressed mRNAs relocate to P-bodies, structures implicated in translational repression and mRNA degradation. Under specific conditions the miRNA repression can be reversed. In response to cellular stress, the repressed CAT-1 mRNA exits P-bodies to reenter translation. The derepression requires binding of the RBP protein HuR to the mRNA 3’UTR. Proteins of the GW182 family emerged recently as particularly important factors involved in miRNA repression in metazoa. They directly interact with Ago proteins, key components of miRNPs, and also form part of P-bodies. Deletion analysis of the human GW182 protein TNRC6C and Drosophila dGW182 revealed that their C-terminal fragments encompassing DUF and RRM domains act as potent mediators of both translational repression and mRNA decay. Features of these C-terminal regions responsible for the repression and factors mediating their function are being characterized. More recently, we also initiated projects aimed towards characterization of miRNAs regulated during light and dark adaptation in the mouse retina (projects carried out in collaboration with Dr. Botond Roska of the Friedrich Miescher Institute). We have identified miRNAs regulated by different light levels in the retina, independent of circadian time. We also characterized mRNA targets which are controlled by the light-regulated miRNAs in vivo. We will discuss possible mechanisms which underlay the light-mediated regulation of miRNA levels in retinal neurons. We will also discuss our recent data on the metabolism of miRNAs in hippocampal and cortical neurons.