Abstract
MicroRNAs play important regulatory roles in a broad range of cellular processes including neuronal morphology and long-term synaptic plasticity. MicroRNA-132 (miR132) is a CREB-regulated miRNA that is induced by neuronal activity and neurotrophins, and plays a role in regulating neuronal morphology and cellular excitability. Little is known about the effects of miR132 expression on synaptic function. Here we show that overexpression of miR132 increases the paired-pulse ratio and decreases synaptic depression in cultured mouse hippocampal neurons without affecting the initial probability of neurotransmitter release, the calcium sensitivity of release, the amplitude of excitatory postsynaptic currents or the size of the readily releasable pool of synaptic vesicles. These findings are the first to demonstrate that microRNAs can regulate short-term plasticity in neurons.
Highlights
While extensive research has explored the role of miRNAs in processes like development and pathogenesis, the function of miRNAs in the adult nervous system is only just beginning to emerge
To achieve overexpression of miR132, we engineered replication-deficient Lentivirus to encode the primary transcript of miR132. These vectors expressed enhanced Green Fluorescent Protein (EGFP) as a separate reporter protein driven by an internal ribosome entry site (IRES)
Control neurons were infected with a Lentivirus that only contained the IRES-EGFP reporter sequence
Summary
While extensive research has explored the role of miRNAs in processes like development and pathogenesis, the function of miRNAs in the adult nervous system is only just beginning to emerge. With their ability to regulate the proteomic composition of neuronal compartments, it stands to reason that miRNAs might play a role in shaping the functional properties of neurons. Upregulation of miR132 increases dendritic outgrowth in an activity-dependent fashion via suppression of a GTPase-activating protein [3,4]. Exposure to light induces transcription of miR132 in the SCN in vivo, where it plays a role in regulating entrainment of the circadian clock [5]
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