SNORD90 induces glutamatergic signaling following treatment with monoaminergic antidepressants.

Autor:	Lin R; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada.; Integrated Program in Neuroscience, McGill University, Montreal, Canada., Kos A; Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel.; Department of Molecular Neuroscience, Weizmann Institute of Science, Rehovot, Israel., Lopez JP; Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel.; Department of Molecular Neuroscience, Weizmann Institute of Science, Rehovot, Israel., Dine J; Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel.; Department of Molecular Neuroscience, Weizmann Institute of Science, Rehovot, Israel., Fiori LM; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada., Yang J; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada., Ben-Efraim Y; Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel.; Department of Molecular Neuroscience, Weizmann Institute of Science, Rehovot, Israel., Aouabed Z; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada., Ibrahim P; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada.; Integrated Program in Neuroscience, McGill University, Montreal, Canada., Mitsuhashi H; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada.; Integrated Program in Neuroscience, McGill University, Montreal, Canada., Wong TP; Neuroscience Division, Douglas Research Centre, Montreal, Canada.; Department of Psychiatry, McGill University, Montreal, Canada., Ibrahim EC; Aix-Marseille Université, CNRS, INT, Institute Neuroscience Timone, Marseille, France., Belzung C; UMR 1253, iBrain, UFR Sciences et Techniques; Parc Grandmont, Tours, France., Blier P; Mood Disorders Research Unit, University of Ottawa Institute of Mental Health Research, Ontario, Canada., Farzan F; eBrain Lab, Simon Fraser University, Columbia, Canada., Frey BN; Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Canada.; Mood Disorders Program, St. Joseph's Healthcare Hamilton, Hamilton, Canada., Lam RW; Department of Psychiatry, University of British Columbia, Columbia, Canada., Milev R; Departments of Psychiatry and Psychology, Queens University, Ontario, Canada., Muller DJ; Department of Psychiatry, University Health Network, Krembil Research Institute, University of Toronto, Toronto, Canada.; Centre for Addiction and Mental Health, Toronto, Canada., Parikh SV; Department of Psychiatry, University of Michigan, Ann Arbor, United States., Soares C; Departments of Psychiatry and Psychology, Queens University, Ontario, Canada., Uher R; Nova Scotia Health Authority, Halifax, Canada.; Department of Psychiatry, Dalhousie University, Halifax, Canada., Nagy C; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada., Mechawar N; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada., Foster JA; Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Canada.; Mood Disorders Program, St. Joseph's Healthcare Hamilton, Hamilton, Canada.; Department of Psychiatry, University Health Network, Krembil Research Institute, University of Toronto, Toronto, Canada., Kennedy SH; Department of Psychiatry, University Health Network, Krembil Research Institute, University of Toronto, Toronto, Canada.; St Michael's Hospital, Li Ka Shing Knowledge Institute, Centre for Depression and Suicide Studies, Toronto, Canada., Chen A; Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.; Department of Brain Sciences, Weizmann Institute of Science, Rehovot, Israel.; Department of Molecular Neuroscience, Weizmann Institute of Science, Rehovot, Israel., Turecki G; McGill Group for Suicide Studies, Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montreal, Canada.
Jazyk:	angličtina
Zdroj:	ELife [Elife] 2023 Jul 11; Vol. 12. Date of Electronic Publication: 2023 Jul 11.
DOI:	10.7554/eLife.85316
Abstrakt:	Pharmacotherapies for the treatment of major depressive disorder were serendipitously discovered almost seven decades ago. From this discovery, scientists pinpointed the monoaminergic system as the primary target associated with symptom alleviation. As a result, most antidepressants have been engineered to act on the monoaminergic system more selectively, primarily on serotonin, in an effort to increase treatment response and reduce unfavorable side effects. However, slow and inconsistent clinical responses continue to be observed with these available treatments. Recent findings point to the glutamatergic system as a target for rapid acting antidepressants. Investigating different cohorts of depressed individuals treated with serotonergic and other monoaminergic antidepressants, we found that the expression of a small nucleolar RNA, SNORD90 , was elevated following treatment response. When we increased Snord90 levels in the mouse anterior cingulate cortex (ACC), a brain region regulating mood responses, we observed antidepressive-like behaviors. We identified neuregulin 3 ( NRG3 ) as one of the targets of SNORD90 , which we show is regulated through the accumulation of N 6 -methyladenosine modifications leading to YTHDF2-mediated RNA decay. We further demonstrate that a decrease in NRG3 expression resulted in increased glutamatergic release in the mouse ACC. These findings support a molecular link between monoaminergic antidepressant treatment and glutamatergic neurotransmission. Competing Interests: RL, AK, JL, JD, LF, JY, YB, ZA, PI, HM, TW, EI, CB, PB, FF, BF, RM, DM, SP, CS, RU, CN, NM, SK, AC, GT No competing interests declared, RL RM has received consulting and speaking honoraria from AbbVie, Allergan, Eisai, Janssen, KYE, Lallemand, Lundbeck, Neomind, Otsuka, and Sunovion, and research grants from CAN-BIND, CIHR, Janssen, Lallemand, Lundbeck, Nubiyota, OBI and OMHF, JF JAF has received consulting and speaking fees from Takeda and RBH, and research funding from NSERC, CIHR, and OBI (© 2023, Lin, Kos et al.)
Databáze:	MEDLINE
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