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Glucocorticoid attenuates brain-derived neurotrophic factor-dependent upregulation of glutamate receptors via the suppression of microRNA-132 expression

Kawashima, H., Numakawa, T., Kumamaru, E., Adachi, N., Mizuno, H., Ninomiya, M., Kunugi, H., Hashido, K.·2010·Neuroscience
DOI 10.1016/j.neuroscience.2009.11.057
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Abstract

Brain-specific microRNAs (miRs) may be involved in synaptic plasticity through the control of target mRNA translation. Brain-derived neurotrophic factor (BDNF) also contributes to the regulation of synaptic function. However, the possible involvement of miRs in BDNF-regulated synaptic function is poorly understood. Importantly, an increase in glucocorticoid levels and the downregulation of BDNF are supposed to be involved in the pathophysiology of depressive disorders. Previously, we reported that glucocorticoid exposure inhibited BDNF-regulated synaptic function via weakening mitogen-activated protein kinase/extracellular signal-regulated kinase1/2 (MAPK/ERK) and/or phospholipase C-gamma (PLC-gamma) intracellular signaling in cultured neurons [Kumamaru et al (2008) Mol Endocrinol 22:546-558; Numakawa et al (2009) Proc Natl Acad Sci U S A 106:647-652]. Therefore, in this study, we investigate the possible influence of glucocorticoid on BDNF/miRs-stimulated biological responses in cultured cortical neurons. Significant upregulation of miR-132 was caused by BDNF, although miR-9, -124, -128a, -128b, -134, -138, and -16 were intact. Transfection of exogenous ds-miR-132 induced marked upregulation of glutamate receptors (NR2A, NR2B, and GluR1), suggesting that miR-132 has a positive effect on the increase in postsynaptic proteins levels. Consistently, transfection of antisense RNA to inhibit miR-132 function decreased the BDNF-dependent increase in the expression of postsynaptic p…

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  • miR-132 can ameliorate AD pathology at multiple levels, through its involvement in TAU metabolism and hyperphosphorylation, amyloidosis, neuronal survival, adult neurogenesis and memory formation.

    “miR-132 can ameliorate AD pathology at multiple levels, through its involvement in TAU metabolism and hyperphosphorylation, amyloidosis, neuronal survival, adult neurogenesis and memory formation [18, 20–34].”

    From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [23]

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Metadata

Authors
Kawashima, H., Numakawa, T., Kumamaru, E., Adachi, N., Mizuno, H., Ninomiya, M., Kunugi, H., & Hashido, K.
Venue
Neuroscience
Publisher
Elsevier BV
Published
2010-02
Volume
165
Issue
4
Pages
1301-1311
ISSN
0306-4522
DOI
10.1016/j.neuroscience.2009.11.057
Cited by
172
References
7
Language
en
Licence
Funders
  • Ichiro Kanehara Foundation
  • Japan Health Sciences Foundation
  • Health and Labor Sciences Research Grants
  • Mitsubishi Pharma Research Foundation
  • Japan Foundation for Neuroscience and Mental Health
  • Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation
  • Ministry of Education, Culture, Sports, Science, and Technology of Japan (21680034)

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