<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pulcrano S</submitter><funding>HHS | NIH | National Institute of Mental Health</funding><funding>Telethon</funding><funding>NINDS NIH HHS</funding><funding>Ministero dell&amp;apos;Università e della Ricerca</funding><pagination>8104-8125</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10697421</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(48)</volume><pubmed_abstract>In the brain, microRNAs (miRNAs) are believed to play a role in orchestrating synaptic plasticity at a higher level by acting as an additional mechanism of translational regulation, alongside the mRNA/polysome system. Despite extensive research, our understanding of the specific contribution of individual miRNA to the function of dopaminergic neurons (DAn) remains limited. By performing a dopaminergic-specific miRNA screening, we have identified miR-218 as a critical regulator of DAn activity in male and female mice. We have found that miR-218 is specifically expressed in mesencephalic DAn and is able to promote dopaminergic differentiation of embryonic stem cells and functional maturation of transdifferentiated induced DA neurons. Midbrain-specific deletion of both genes encoding for miR-</pubmed_abstract><journal>The Journal of neuroscience : the official journal of the Society for Neuroscience</journal><pubmed_title>miR-218 Promotes Dopaminergic Differentiation and Controls Neuron Excitability and Neurotransmitter Release through the Regulation of a Synaptic-Related Genes Network.</pubmed_title><pmcid>PMC10697421</pmcid><funding_grant_id>R01 NS119690</funding_grant_id><funding_grant_id>R01NS119690</funding_grant_id><funding_grant_id>TMDMMFU22TT</funding_grant_id><funding_grant_id>PRIN 2017T9JNLT_004</funding_grant_id><pubmed_authors>Speranza L</pubmed_authors><pubmed_authors>Volpicelli F</pubmed_authors><pubmed_authors>Guatteo E</pubmed_authors><pubmed_authors>Pulcrano S</pubmed_authors><pubmed_authors>De Gregorio R</pubmed_authors><pubmed_authors>Perrone-Capano C</pubmed_authors><pubmed_authors>Piscitelli RM</pubmed_authors><pubmed_authors>Giacomet C</pubmed_authors><pubmed_authors>Mercuri NB</pubmed_authors><pubmed_authors>De Sanctis C</pubmed_authors><pubmed_authors>Martini A</pubmed_authors><pubmed_authors>Awatramani R</pubmed_authors><pubmed_authors>Federici M</pubmed_authors><pubmed_authors>di Porzio U</pubmed_authors><pubmed_authors>Caiazzo M</pubmed_authors><pubmed_authors>Medina D</pubmed_authors><pubmed_authors>Bellenchi GC</pubmed_authors><pubmed_authors>Viggiano D</pubmed_authors></additional><is_claimable>false</is_claimable><name>miR-218 Promotes Dopaminergic Differentiation and Controls Neuron Excitability and Neurotransmitter Release through the Regulation of a Synaptic-Related Genes Network.</name><description>In the brain, microRNAs (miRNAs) are believed to play a role in orchestrating synaptic plasticity at a higher level by acting as an additional mechanism of translational regulation, alongside the mRNA/polysome system. Despite extensive research, our understanding of the specific contribution of individual miRNA to the function of dopaminergic neurons (DAn) remains limited. By performing a dopaminergic-specific miRNA screening, we have identified miR-218 as a critical regulator of DAn activity in male and female mice. We have found that miR-218 is specifically expressed in mesencephalic DAn and is able to promote dopaminergic differentiation of embryonic stem cells and functional maturation of transdifferentiated induced DA neurons. Midbrain-specific deletion of both genes encoding for miR-</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2026-05-23T03:15:22.712Z</modification><creation>2026-05-23T03:08:06.248Z</creation></dates><accession>S-EPMC10697421</accession><cross_references><pubmed>37816598</pubmed><doi>10.1523/jneurosci.0431-23.2023</doi><doi>10.1523/JNEUROSCI.0431-23.2023</doi></cross_references></HashMap>