A Role for mir-26a in Stress: A Potential sEV Biomarker and Modulator of Excitatory Neurotransmission
Author
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Lafourcade, Carlos Andrés
Author
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Fernández, Anllely
Author
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Ramírez, Juan Pablo
Author
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Corvalán, Katherine
Author
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Carrasco, Miguel Ángel
Author
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Iturriaga, Andrés
Author
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Bátiz, Luis Federico
Author
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Luarte, Alejandro
Author
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Wyneken, Úrsula
Admission date
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2020-10-01T23:21:46Z
Available date
dc.date.available
2020-10-01T23:21:46Z
Publication date
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2020
Cita de ítem
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Cells 2020, 9, 1364
es_ES
Identifier
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10.3390/cells9061364
Identifier
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https://repositorio.uchile.cl/handle/2250/176950
Abstract
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Stress is a widespread problem in today's societies, having important consequences on brain function. Among the plethora of mechanisms involved in the stress response at the molecular level, the role of microRNAs (miRNAs) is beginning to be recognized. The control of gene expression by these noncoding RNAs makes them essential regulators of neuronal and synaptic physiology, and alterations in their levels have been associated with pathological conditions and mental disorders. In particular, the excitatory (i.e., glutamate-mediated) neurotransmission is importantly affected by stress. Here, we found that loss of miR-26a-5p (miR-26a henceforth) function in primary hippocampal neurons increased the frequency and amplitude of miniature excitatory currents, as well as the expression levels of the excitatory postsynaptic scaffolding protein PSD95. Incubation of primary hippocampal neurons with corticosterone downregulated miR-26a, an effect that mirrored our in vivo results, as miR-26a was downregulated in the hippocampus as well as in blood serum-derived small extracellular vesicles (sEVs) of rats exposed to two different stress paradigms by movement restriction (i.e., stress by restraint in cages or by complete immobilization in bags). Overall, these results suggest that miR-26a may be involved in the generalized stress response and that a stress-induced downregulation of miR-26a could have long-term effects on glutamate neurotransmission.
es_ES
Patrocinador
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Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
CONICYT FONDECYT
1200693