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Updated: Apr 4, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
Published on: March 16, 2017
Interplay Between Nitric Oxide and Brain-Derived Neurotrophic Factor in Neuronal Plasticity
Caroline Biojone1, Plinio Cabrera Casarotto, Samia Regiane Joca
1Neuroscience Center, University of Helsinki, Viikinkaari 4, 00790, Helsinki, Finland. caroline.biojone@helsinki.fi.
Nitric oxide (NO) and brain-derived neurotrophic factor (BDNF) interact in the central nervous system. This review explores their relationship and proposes NO may directly modify BDNF receptors, impacting neuronal function.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Nitric oxide (NO) is a key neuromodulator in the central nervous system, influencing neurotransmitter release, cell differentiation, and maturation.
- NO's mechanisms involve soluble guanylate cyclase activation and protein modification via nitration/S-nitrosylation.
- Brain-derived neurotrophic factor (BDNF), acting via its receptor Tropomyosin-related kinase B (TrkB), is vital for neuronal survival, differentiation, and synaptic plasticity.
Purpose of the Study:
- To review the existing evidence on the interaction between nitric oxide and brain-derived neurotrophic factor.
- To propose a potential direct molecular mechanism linking NO and BDNF signaling pathways.
Main Methods:
- Literature review of studies investigating NO and BDNF.
- Bioinformatics analysis of amino acid sequences for BDNF and TrkB receptors.
Main Results:
- NO regulates BDNF production and signaling pathways.
- Bioinformatics analysis suggests NO may directly nitrate or S-nitrosylate BDNF and/or its receptors (TrkB).
Conclusions:
- The interaction between NO and BDNF is complex and bidirectional.
- A putative direct action of NO on BDNF/TrkB signaling warrants further experimental investigation to elucidate novel therapeutic targets.
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