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Nitric Oxide Signaling Strengthens Inhibitory Synapses of Cerebellar Molecular Layer Interneurons through a GABARAP-Dependent Mechanism.

التفاصيل البيبلوغرافية
العنوان: Nitric Oxide Signaling Strengthens Inhibitory Synapses of Cerebellar Molecular Layer Interneurons through a GABARAP-Dependent Mechanism.
المؤلفون: Larson EA; Integrated Program in Neuroscience, McGill University, Montréal, Québec, Canada H3A 2B4.; Department of Pharmacology and Therapeutics, McGill University, Montréal H3G 0B1, Québec, Canada., Accardi MV; Graduate Program in Pharmacology, McGill University, Montréal, Québec, Canada H3G 1Y6.; Department of Pharmacology and Therapeutics, McGill University, Montréal H3G 0B1, Québec, Canada., Wang Y; Department of Physiology and Pathophysiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0J9.; Neuroscience Research Program, Kleysen Institute for Advanced Medicine, Health Sciences Centre, Winnipeg, Manitoba, Canada R3E 3J7.; The Children's Hospital Research Institute of Manitoba, Winnipeg, Manitoba Canada R3E 3P4., D'Antoni M; Integrated Program in Neuroscience, McGill University, Montréal, Québec, Canada H3A 2B4.; Department of Pharmacology and Therapeutics, McGill University, Montréal H3G 0B1, Québec, Canada., Karimi B; Department of Physiology and Pathophysiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0J9.; Neuroscience Research Program, Kleysen Institute for Advanced Medicine, Health Sciences Centre, Winnipeg, Manitoba, Canada R3E 3J7.; The Children's Hospital Research Institute of Manitoba, Winnipeg, Manitoba Canada R3E 3P4., Siddiqui TJ; Department of Physiology and Pathophysiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0J9.; Neuroscience Research Program, Kleysen Institute for Advanced Medicine, Health Sciences Centre, Winnipeg, Manitoba, Canada R3E 3J7.; The Children's Hospital Research Institute of Manitoba, Winnipeg, Manitoba Canada R3E 3P4., Bowie D; Department of Pharmacology and Therapeutics, McGill University, Montréal H3G 0B1, Québec, Canada derek.bowie@mcgill.ca.
المصدر: The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 2020 Apr 22; Vol. 40 (17), pp. 3348-3359. Date of Electronic Publication: 2020 Mar 13.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Society for Neuroscience Country of Publication: United States NLM ID: 8102140 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1529-2401 (Electronic) Linking ISSN: 02706474 NLM ISO Abbreviation: J Neurosci Subsets: MEDLINE
أسماء مطبوعة: Publication: Washington, DC : Society for Neuroscience
Original Publication: [Baltimore, Md.] : The Society, c1981-
مواضيع طبية MeSH: Apoptosis Regulatory Proteins/*metabolism , Cerebellum/*metabolism , Interneurons/*metabolism , Microtubule-Associated Proteins/*metabolism , Nitric Oxide/*metabolism , Signal Transduction/*physiology, Animals ; Cerebellum/drug effects ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Female ; Interneurons/drug effects ; Male ; Mice ; Neural Inhibition/drug effects ; Neural Inhibition/physiology ; Nitric Oxide Synthase Type I/antagonists & inhibitors ; Patch-Clamp Techniques ; Signal Transduction/drug effects ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology
مستخلص: Nitric oxide (NO) is an important signaling molecule that fulfills diverse functional roles as a neurotransmitter or diffusible second messenger in the developing and adult CNS. Although the impact of NO on different behaviors such as movement, sleep, learning, and memory has been well documented, the identity of its molecular and cellular targets is still an area of ongoing investigation. Here, we identify a novel role for NO in strengthening inhibitory GABA A receptor-mediated transmission in molecular layer interneurons of the mouse cerebellum. NO levels are elevated by the activity of neuronal NO synthase (nNOS) following Ca 2+ entry through extrasynaptic NMDA-type ionotropic glutamate receptors (NMDARs). NO activates protein kinase G with the subsequent production of cGMP, which prompts the stimulation of NADPH oxidase and protein kinase C (PKC). The activation of PKC promotes the selective strengthening of α3-containing GABA A Rs synapses through a GΑΒΑ receptor-associated protein-dependent mechanism. Given the widespread but cell type-specific expression of the NMDAR/nNOS complex in the mammalian brain, our data suggest that NMDARs may uniquely strengthen inhibitory GABAergic transmission in these cells through a novel NO-mediated pathway. SIGNIFICANCE STATEMENT Long-term changes in the efficacy of GABAergic transmission is mediated by multiple presynaptic and postsynaptic mechanisms. A prominent pathway involves crosstalk between excitatory and inhibitory synapses whereby Ca 2+ -entering through postsynaptic NMDARs promotes the recruitment and strengthening of GABA A receptor synapses via Ca 2+ /calmodulin-dependent protein kinase II. Although Ca 2+ transport by NMDARs is also tightly coupled to nNOS activity and NO production, it has yet to be determined whether this pathway affects inhibitory synapses. Here, we show that activation of NMDARs trigger a NO-dependent pathway that strengthens inhibitory GABAergic synapses of cerebellar molecular layer interneurons. Given the widespread expression of NMDARs and nNOS in the mammalian brain, we speculate that NO control of GABAergic synapse efficacy may be more widespread than has been appreciated.
(Copyright © 2020 the authors.)
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معلومات مُعتمدة: MOP-342247 Canada CIHR; MOP-142209 Canada CIHR
فهرسة مساهمة: Keywords: GABA receptor; GABARAP; cerebellum; electrophysiology; inhibitory synapse; plasticity
المشرفين على المادة: 0 (Apoptosis Regulatory Proteins)
0 (Enzyme Inhibitors)
0 (Excitatory Amino Acid Antagonists)
0 (GABARAP protein, mouse)
0 (Microtubule-Associated Proteins)
31C4KY9ESH (Nitric Oxide)
EC 1.14.13.39 (Nitric Oxide Synthase Type I)
تواريخ الأحداث: Date Created: 20200315 Date Completed: 20200923 Latest Revision: 20201022
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC7178912
DOI: 10.1523/JNEUROSCI.2211-19.2020
PMID: 32169968
قاعدة البيانات: MEDLINE
الوصف
تدمد:1529-2401
DOI:10.1523/JNEUROSCI.2211-19.2020