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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...

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Differentiation of a Human Neural Stem Cell Line on Three Dimensional Cultures, Analysis of MicroRNA and Putative Target Genes

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MicroRNA-101 Regulates Multiple Developmental Programs to Constrain Excitation in Adult Neural Networks.

Giordano Lippi¹, Catarina C Fernandes¹, Laura A Ewell¹

¹Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.

|December 13, 2016

Summary

This summary is machine-generated.

MicroRNA-101 (miR-101) balances neural network excitation and inhibition. Blocking miR-101 early causes lasting hyper-excitability and memory deficits, revealing its crucial role in brain development.

Keywords:

GABA switch NKCC1 excitation/inhibition (E/I)hyper-excitability miR-101 microRNA network development neurodevelopmental disorders synaptogenesis target-site blockers

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Assaying Circuit Specific Regulation of Adult Hippocampal Neural Precursor Cells

Assaying Circuit Specific Regulation of Adult Hippocampal Neural Precursor Cells

Published on: July 24, 2019

Area of Science:

Neuroscience
Molecular Biology
Developmental Biology

Background:

Neural network function relies on a balance between excitation and inhibition.
Dysregulation of this balance is implicated in neurological disorders.
The mechanisms governing this critical balance during development are largely unknown.

Purpose of the Study:

To investigate the role of microRNA-101 (miR-101) in orchestrating neural network excitation-inhibition balance.
To identify developmental programs regulated by miR-101 that shape network function.
To explore miR-101 as a potential therapeutic target for neurological dysfunction.

Main Methods:

Utilized in vivo target site blockers to manipulate miR-101 activity during development.
Analyzed the impact of miR-101 blockade on neural excitability and memory.
Identified and validated key developmental targets of miR-101, including NKCC1, Kif1a, and Ank2.

Main Results:

Early blockade of miR-101 led to persistent hyper-excitability and memory deficits.
miR-101 regulates multiple parallel developmental programs essential for balanced neural networks.
miR-101 repression of NKCC1 influences GABA signaling and limits early neuronal activity and dendritic growth.
miR-101 targets Kif1a and Ank2 to prevent excessive synapse formation.

Conclusions:

miR-101 is a critical regulator of the excitation-inhibition balance in developing neural networks.
Simultaneous de-repression of NKCC1, Kif1a, and Ank2 recapitulates the major dysfunctions caused by miR-101 blockade.
These findings offer mechanistic insights into brain development and identify potential therapeutic targets for neurological disorders.