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MicroRNA-128 Governs Neuronal Excitability and Motor Behavior in Mice
Abstract
Not Too Much, Not Too Little: The microRNA miR128 is expressed in brain neurons of the mouse. Lek Tan et al. (p. 1254 ) now find that miR128 is crucial to stable brain function. Mice deficient in miR128 developed hyperactivity and were susceptible to fatal seizures, whereas overexpression of miR128 correlated with reduced motor activity and reduced susceptibility to proconvulsive drugs. Experiments using ex vivo–isolated adult brain tissues suggested that miR-128 controlled motor activity by governing the signaling network that determines the intrinsic excitability and signal responsiveness of neurons.
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Previous studies have confirmed that when expressed in the mouse brain, FLAG-Ago2 carries an extensive range of miRNAs representative of the functional miRNA pool.
“Previous studies have confirmed that when expressed in the mouse brain, FLAG-Ago2 carries an extensive range of miRNAs representative of the functional miRNA pool (Schaefer et al., 2010; Tan et al., 2013; Brennan et al., 2020).”
From Brain cell-specific origin of circulating microRNA biomarkers in experimental temporal lobe epilepsy (2023) · cites this paper as Tan et al., 2013
In mice, the mmu-MIR128-2 locus is responsible for generating a majority of mature mmu-miR-128-3p.
“Interestingly, Tan et al. demonstrated that the mmu-MIR128-2 locus is responsible for generating a majority of mature mmu-miR-128-3p in mice29”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
Animal model studies showed that miR-128-3p regulates motor behavior by modulating neuronal signaling networks and excitability.
“Animal model studies showed that miR-128-3p regulates motor behavior by modulating neuronal signaling networks and excitability.”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
Ion channels and transporters are critical for maintaining the electrical activity of neurons that contribute to neuronal excitability and neurotransmitter-driven motor activity.
“which are critical for maintaining the electrical activity of neurons that contribute to neuronal excitability and neurotransmitter-driven motor activity.”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
MiR-128-3p is significantly lower in astrocytes and oligodendrocytes.
“while its significantly lower level was shown in astrocytes and oligodendrocytes.29”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
Conditional deletion of both miR-128-3p forms in postnatal neurons in mice resulted in fatal epilepsy.
“Conditional deletion of both miR-128-3p forms in postnatal neurons in mice resulted in fatal epilepsy.”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
miR-128-3p is prominently observed in differentiating neuronal cells.
“being prominently observed in differentiating neuronal cells29,31”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
MiR-128-3p regulates the expression of many genes, including genes encoding ion channels and transporters.
“MiR-128-3p regulates the expression of many genes, including those encoding for ion channels and transporters”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
miR-128-3p targets synaptic plasticity and memory-related genes such as CREB1 and NRXN1, and genes encoding ion channel and transporter subunits like the BK channel.
“Additionally, miR-128-3p targets synaptic plasticity and memory-related genes, such as CREB1 (CAMP Responsive element binding protein 1) or NRXN1 (Neurexin 1),142 and genes encoding subunits of ion channels and transporters like the Big Potassium (BK) channel.29”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [29]
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Citations
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Metadata
- Authors
- Tan, C. L., Plotkin, J. L., Venø, M. T., von Schimmelmann, M., Feinberg, P., Mann, S., Handler, A., Kjems, J., Surmeier, D. J., O’Carroll, D., Greengard, P., & Schaefer, A.
- Affiliations
- Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10065, USA.
- Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
- Interdisciplinary Nanoscience Center (iNANO) and Department of Molecular Biology and Genetics, Faculty of Science, Aarhus University, DK-8000 Aarhus, Denmark.
- European Molecular Biology Laboratory, Mouse Biology Unit, Via Ramarini 32, Monterotondo Scalo 00015, Italy.
- Venue
- Science
- Published
- 2013-12-06
- Volume
- 342
- Issue
- 6163
- Pages
- 1254-1258
- ISSN
- 0036-8075
- 1095-9203
- PMC
- PMC3932786
- Cited by
- 301
- References
- 8
- Language
- en
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