MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction. / Kocerha, Jannet; Faghihi, Mohammad Ali; Lopez-Toledano, Miguel A; Huang, Jia; Ramsey, Amy J; Caron, Marc G; Sales, Nicole; Willoughby, David; Elmen, Joacim; Hansen, Henrik F; Orum, Henrik; Kauppinen, Sakari; Kenny, Paul J; Wahlestedt, Claes.

In: Proceedings of the National Academy of Science of the United States of America, Vol. 106, No. 9, 2009, p. 3507-12.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Kocerha, J, Faghihi, MA, Lopez-Toledano, MA, Huang, J, Ramsey, AJ, Caron, MG, Sales, N, Willoughby, D, Elmen, J, Hansen, HF, Orum, H, Kauppinen, S, Kenny, PJ & Wahlestedt, C 2009, 'MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction', Proceedings of the National Academy of Science of the United States of America, vol. 106, no. 9, pp. 3507-12. https://doi.org/10.1073/pnas.0805854106

APA

Kocerha, J., Faghihi, M. A., Lopez-Toledano, M. A., Huang, J., Ramsey, A. J., Caron, M. G., Sales, N., Willoughby, D., Elmen, J., Hansen, H. F., Orum, H., Kauppinen, S., Kenny, P. J., & Wahlestedt, C. (2009). MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction. Proceedings of the National Academy of Science of the United States of America, 106(9), 3507-12. https://doi.org/10.1073/pnas.0805854106

Vancouver

Kocerha J, Faghihi MA, Lopez-Toledano MA, Huang J, Ramsey AJ, Caron MG et al. MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction. Proceedings of the National Academy of Science of the United States of America. 2009;106(9):3507-12. https://doi.org/10.1073/pnas.0805854106

Author

Kocerha, Jannet ; Faghihi, Mohammad Ali ; Lopez-Toledano, Miguel A ; Huang, Jia ; Ramsey, Amy J ; Caron, Marc G ; Sales, Nicole ; Willoughby, David ; Elmen, Joacim ; Hansen, Henrik F ; Orum, Henrik ; Kauppinen, Sakari ; Kenny, Paul J ; Wahlestedt, Claes. / MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction. In: Proceedings of the National Academy of Science of the United States of America. 2009 ; Vol. 106, No. 9. pp. 3507-12.

Bibtex

@article{49738af090ba11df928f000ea68e967b,
title = "MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction",
abstract = "N-methyl-D-aspartate (NMDA) glutamate receptors are regulators of fast neurotransmission and synaptic plasticity in the brain. Disruption of NMDA-mediated glutamate signaling has been linked to behavioral deficits displayed in psychiatric disorders such as schizophrenia. Recently, noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators of neuronal functions. Here we show that pharmacological (dizocilpine) or genetic (NR1 hypomorphism) disruption of NMDA receptor signaling reduces levels of a brain-specific miRNA, miR-219, in the prefrontal cortex (PFC) of mice. Consistent with a role for miR-219 in NMDA receptor signaling, we identify calcium/calmodulin-dependent protein kinase II gamma subunit (CaMKIIgamma), a component of the NMDA receptor signaling cascade, as a target of miR-219. In vivo inhibition of miR-219 by specific antimiR in the murine brain significantly modulated behavioral responses associated with disrupted NMDA receptor transmission. Furthermore, pretreatment with the antipsychotic drugs haloperidol and clozapine prevented dizocilpine-induced effects on miR-219. Taken together, these data support an integral role for miR-219 in the expression of behavioral aberrations associated with NMDA receptor hypofunction.",
author = "Jannet Kocerha and Faghihi, {Mohammad Ali} and Lopez-Toledano, {Miguel A} and Jia Huang and Ramsey, {Amy J} and Caron, {Marc G} and Nicole Sales and David Willoughby and Joacim Elmen and Hansen, {Henrik F} and Henrik Orum and Sakari Kauppinen and Kenny, {Paul J} and Claes Wahlestedt",
note = "Keywords: Animals; Behavior, Animal; Biological Transport; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cell Line, Tumor; Dizocilpine Maleate; Gene Expression Regulation; Gene Therapy; Male; Mice; Mice, Inbred C57BL; MicroRNAs; Nervous System Diseases; Protein Subunits; RNA, Messenger; Receptors, N-Methyl-D-Aspartate; Signal Transduction",
year = "2009",
doi = "10.1073/pnas.0805854106",
language = "English",
volume = "106",
pages = "3507--12",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "The National Academy of Sciences of the United States of America",
number = "9",

}

RIS

TY - JOUR

T1 - MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction

AU - Kocerha, Jannet

AU - Faghihi, Mohammad Ali

AU - Lopez-Toledano, Miguel A

AU - Huang, Jia

AU - Ramsey, Amy J

AU - Caron, Marc G

AU - Sales, Nicole

AU - Willoughby, David

AU - Elmen, Joacim

AU - Hansen, Henrik F

AU - Orum, Henrik

AU - Kauppinen, Sakari

AU - Kenny, Paul J

AU - Wahlestedt, Claes

N1 - Keywords: Animals; Behavior, Animal; Biological Transport; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cell Line, Tumor; Dizocilpine Maleate; Gene Expression Regulation; Gene Therapy; Male; Mice; Mice, Inbred C57BL; MicroRNAs; Nervous System Diseases; Protein Subunits; RNA, Messenger; Receptors, N-Methyl-D-Aspartate; Signal Transduction

PY - 2009

Y1 - 2009

N2 - N-methyl-D-aspartate (NMDA) glutamate receptors are regulators of fast neurotransmission and synaptic plasticity in the brain. Disruption of NMDA-mediated glutamate signaling has been linked to behavioral deficits displayed in psychiatric disorders such as schizophrenia. Recently, noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators of neuronal functions. Here we show that pharmacological (dizocilpine) or genetic (NR1 hypomorphism) disruption of NMDA receptor signaling reduces levels of a brain-specific miRNA, miR-219, in the prefrontal cortex (PFC) of mice. Consistent with a role for miR-219 in NMDA receptor signaling, we identify calcium/calmodulin-dependent protein kinase II gamma subunit (CaMKIIgamma), a component of the NMDA receptor signaling cascade, as a target of miR-219. In vivo inhibition of miR-219 by specific antimiR in the murine brain significantly modulated behavioral responses associated with disrupted NMDA receptor transmission. Furthermore, pretreatment with the antipsychotic drugs haloperidol and clozapine prevented dizocilpine-induced effects on miR-219. Taken together, these data support an integral role for miR-219 in the expression of behavioral aberrations associated with NMDA receptor hypofunction.

AB - N-methyl-D-aspartate (NMDA) glutamate receptors are regulators of fast neurotransmission and synaptic plasticity in the brain. Disruption of NMDA-mediated glutamate signaling has been linked to behavioral deficits displayed in psychiatric disorders such as schizophrenia. Recently, noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators of neuronal functions. Here we show that pharmacological (dizocilpine) or genetic (NR1 hypomorphism) disruption of NMDA receptor signaling reduces levels of a brain-specific miRNA, miR-219, in the prefrontal cortex (PFC) of mice. Consistent with a role for miR-219 in NMDA receptor signaling, we identify calcium/calmodulin-dependent protein kinase II gamma subunit (CaMKIIgamma), a component of the NMDA receptor signaling cascade, as a target of miR-219. In vivo inhibition of miR-219 by specific antimiR in the murine brain significantly modulated behavioral responses associated with disrupted NMDA receptor transmission. Furthermore, pretreatment with the antipsychotic drugs haloperidol and clozapine prevented dizocilpine-induced effects on miR-219. Taken together, these data support an integral role for miR-219 in the expression of behavioral aberrations associated with NMDA receptor hypofunction.

U2 - 10.1073/pnas.0805854106

DO - 10.1073/pnas.0805854106

M3 - Journal article

C2 - 19196972

VL - 106

SP - 3507

EP - 3512

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 9

ER -

ID: 20876124