ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Tonic and phasic nitric oxide signals in hippocampal long-term potentiation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 233 citations in OpenAlex.
- Nitric oxide as a mechanistic link between metabolic dysfunction and cognitive decline in type 2 diabetes.Biochemical Society transactions · 2026Review
- Severity-dependent changes in hippocampal necroptosis markers and neuronal loss in a PTSD-like mouse model: potential involvement of nitric oxide signaling.Psychopharmacology · 2026Article
- Voltage-Dependent Ion Channels in Vascular Endothelial Cells: An Unexpected Signaling Pathway in Non-Excitable Cells.Biomedicines · 2026Review
- Radical Revelations: The Interplay of Nitrosative Stress, the Endocannabinoid System, and Treatment of Age-Related Disorders.International journal of molecular sciences · 2026Review
- Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease.Brain sciences · 2025Review
- Cerebrovascular-mediated dynamic alterations in neurovascular coupling: a key pathological mechanism of depression.Cell & bioscience · 2025Review
- Cognitive Impairment and Synaptic Dysfunction in Cardiovascular Disorders: The New Frontiers of the Heart-Brain Axis.Biomedicines · 2024Review
- The Unexpected Role of the Endothelial Nitric Oxide Synthase at the Neurovascular Unit: Beyond the Regulation of Cerebral Blood Flow.International journal of molecular sciences · 2024Review
- nNOS and Neurological, Neuropsychiatric Disorders: A 20-Year Story.Neuroscience bulletin · 2023Review
- Review
- The Emerging Role of N-Methyl-D-Aspartate (NMDA) Receptors in the Cardiovascular System: Physiological Implications, Pathological Consequences, and Therapeutic Perspectives.International journal of molecular sciences · 2023Review
- Molecular mechanisms underlying physical exercise-induced brain BDNF overproduction.Frontiers in molecular neuroscience · 2023Review
- Changes in brain perfusion with training-related visuomotor improvement in MS.Frontiers in molecular neuroscience · 2023Article
- Acute deletion of the central MR/GR steroid receptor correlates with changes in LTP, auditory neural gain, and GC-A cGMP signaling.Frontiers in molecular neuroscience · 2023Article
- Learning and memory impairment induced by 1,4-butanediol is regulated by ERK1/2-CREB-BDNF signaling pathways in PC12 cells.Metabolic brain disease · 2022Article
- Region-Dependent Increase of Cerebral Blood Flow During Electrically Induced Contraction of the Hindlimbs in Rats.Frontiers in physiology · 2022Article
- Long-term depression-related tau phosphorylation is enhanced by methylene blue in healthy rat hippocampus.Pharmacological reports : PR · 2021Article
- Understanding the heart-brain axis response in COVID-19 patients: A suggestive perspective for therapeutic development.Pharmacological research · 2021Review
- The Roles of Nitric Oxide Synthase/Nitric Oxide Pathway in the Pathology of Vascular Dementia and Related Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Nitric oxide and the brain. Part 2: Effects following neonatal brain injury-friend or foe?Pediatric research · 2021Review
21 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) participates in long-term potentiation (LTP) and other forms of synaptic plasticity in many different brain areas but where it comes from and how it acts remain controversial. Using rat and mouse hippocampal slices, we tested the hypothesis that tonic and phasic NO signals are needed and that they derive from different NO synthase isoforms. NMDA increased NO production in a manner that was potently inhibited by three different neuronal NO synthase (nNOS) inhibitors. Tonic NO could be monitored after sensitizing guanylyl cyclase-coupled NO receptors, allowing the very low ambient NO concentrations to be detected by cGMP measurement. The levels were unaffected by inhibition of NMDA receptors, nNOS, or the inducible NO synthase (iNOS). iNOS was also undetectable in protein or activity assays. Tonic NO was susceptible to agents inhibiting endothelial NO synthase (eNOS) and was missing in eNOS knock-out mice. The eNOS knock-outs exhibited a deficiency in LTP resembling that seen in wild-types treated with a NO synthase inhibitor. LTP in the knock-outs could be fully restored by supplying a low level of NO exogenously. Inhibition of nNOS also caused a major loss of LTP, particularly of late-LTP. Again, exogenous NO could compensate, but higher concentrations were needed compared with those restoring LTP in the eNOS knock-outs. It is concluded that tonic and phasic NO signals are both required for hippocampal LTP and the two are generated, respectively, by eNOS and nNOS, the former in blood vessels and the latter in neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.