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Dysregulation of miRNAs Levels in Glycogen Synthase Kinase-3β Overexpressing Mice and the Role of miR-221-5p in Synaptic Function. | LitMetric

Dysregulation of miRNAs Levels in Glycogen Synthase Kinase-3β Overexpressing Mice and the Role of miR-221-5p in Synaptic Function.

Neuroscience

Laboratory of Electrophysiology, Nencki Institute of Experimental Biology, PAS, Warsaw, Poland; Laboratory of Neurobiology, BRAINCITY, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur Street, 02-093 Warsaw, Poland.

Published: May 2022

AI Article Synopsis

  • - Glycogen synthase kinase-3β (GSK-3β) is crucial for brain function and synaptic plasticity, but its abnormal activity is linked to various neurological and psychiatric diseases.
  • - In mice, overexpression of a more active form of GSK-3β (GSK-3β[S9A]) mimics cognitive and structural issues similar to those found in these disorders, suggesting a role in synaptic dysfunction.
  • - The study found that GSK-3β overactivity lowers levels of certain miRNAs, particularly miR-221-5p, which increases excitatory synaptic transmission in hippocampal neurons, highlighting a potential mechanism for how GSK-3β affects syn

Article Abstract

Glycogen synthase kinase-3β (GSK-3β) is a highly expressed kinase in the brain, where it has an important role in synaptic plasticity. Aberrant activity of GSK-3β leads to synaptic dysfunction which results in the development of several neuropsychiatric and neurological diseases. Notably, overexpression of constitutively active form of GSK-3β (GSK-3β[S9A]) in mice recapitulates the cognitive and structural defects characteristic for neurological and psychiatric disorders. However, the mechanisms by which GSK-3β regulates synaptic functions are not clearly known. Here, we investigate the effects of GSK-3β overactivity on neuronal miRNA expression in the mouse hippocampus. We found that GSK-3β overactivity downregulates miRNA network with a potent effect on miR-221-5p (miR-221*). Next, characterization of miR-221* function in primary hippocampal cell culture transfected by miR-221* inhibitor, showed no structural changes in dendritic spine shape and density. Using electrophysiological methods, we found that downregulation of miR-221* increases excitatory synaptic transmission in hippocampal neurons, probably via postsynaptic mechanisms. Thus, our data reveal potential mechanism by which GSK-3β and miRNAs might regulate synaptic function and therefore also synaptic plasticity.

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Source
http://dx.doi.org/10.1016/j.neuroscience.2022.03.024DOI Listing

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