ArticleFrontiers in synaptic neuroscience2016
Nitric Oxide Is Required for L-Type Ca(2+) Channel-Dependent Long-Term Potentiation in the Hippocampus.
Article in Frontiers in synaptic neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- Atorvastatin improves long-term memory by reducing amyloid-β formation and neuronal damage in STZ-induced diabetic rats.Journal of molecular histology · 2025Article
- Modulatory effect of olanzapine on neuronal nitric oxide synthase (nNOS) expression in the rat striatum.Journal of neural transmission (Vienna, Austria : 1996) · 2024Article
- Per-ARNT-Sim Domains in Nitric Oxide Signaling by Soluble Guanylyl Cyclase.Journal of molecular biology · 2024Review
- Nitric Oxide Synthase Blockade Impairs Spontaneous Calcium Activity in Mouse Primary Hippocampal Culture Cells.International journal of molecular sciences · 2023Article
- Comparative assessment of the effects of DREADDs and endogenously expressed GPCRs in hippocampal astrocytes on synaptic activity and memory.Frontiers in cellular neuroscience · 2023Review
- Protection against Morphine-Induced Inhibitory Avoidance Memory Impairment in Rat by Curcumin: Possible Role of Nitric Oxide/ cAMP-Response Element Binding Protein Pathway.Iranian journal of medical sciences · 2022Article
- Effects of Ethanolic Extract of Cynara cardunculus (Artichoke) Leaves on Neuroinflammatory and Neurochemical Parameters in a Diet-Induced Mice Obesity Model.Neurochemical research · 2022Article
- Metformin attenuates sepsis-induced neuronal injury and cognitive impairment.BMC neuroscience · 2021Article
- Nitric Oxide-Dependent Mechanisms Underlying MK-801- or Scopolamine-Induced Memory Dysfunction in Animals: Mechanistic Studies.International journal of molecular sciences · 2021Article
- Extracellular Metalloproteinases in the Plasticity of Excitatory and Inhibitory Synapses.Cells · 2021Review
- Early and Delayed Impact of Nanosilver on the Glutamatergic NMDA Receptor Complex in Immature Rat Brain.International journal of molecular sciences · 2021Article
- Inhibition of neuroinflammatory nitric oxide signaling suppresses glycation and prevents neuronal dysfunction in mouse prion disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Nitric Oxide Signaling in the Auditory Pathway.Frontiers in neural circuits · 2021Review
- Astrocyte-mediated switch in spike timing-dependent plasticity during hippocampal development.Nature communications · 2020Article
- L-type CaScience signaling · 2020Article
- Modulation of AMPA Receptors by Nitric Oxide in Nerve Cells.International journal of molecular sciences · 2020Review
- Unifying Long-Term Plasticity Rules for Excitatory Synapses by Modeling Dendrites of Cortical Pyramidal Neurons.Cell reports · 2019Article
- Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: A Steered-Glutamatergic Perspective.Brain sciences · 2019Review
- Akt phosphorylation of neuronal nitric oxide synthase regulates gastrointestinal motility in mouse ileum.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Nitric Oxide Donor Prevents Neonatal Isoflurane-induced Impairments in Synaptic Plasticity and Memory.Anesthesiology · 2019Article
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Authors and funding
2 authors at 2 institutions in 1 country.
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Abstract
Nitric oxide (NO) has long been implicated in the generation of long-term potentiation (LTP) and other types of synaptic plasticity, a role for which the intimate coupling between NMDA receptors (NMDARs) and the neuronal isoform of NO synthase (nNOS) is likely to be instrumental in many instances. While several types of synaptic plasticity depend on NMDARs, others do not, an example of which is LTP triggered by opening of L-type voltage-gated Ca(2+) channels (L-VGCCs) in postsynaptic neurons. In CA3-CA1 synapses in the hippocampus, NMDAR-dependent LTP (LTPNMDAR) appears to be primarily expressed postsynaptically whereas L-VGCC-dependent LTP (LTPL-VGCC), which often coexists with LTPNMDAR, appears mainly to reflect enhanced presynaptic transmitter release. Since NO is an excellent candidate as a retrograde messenger mediating post-to-presynaptic signaling, we sought to determine if NO functions in LTPL-VGCC in mouse CA3-CA1 synapses. When elicited by a burst type of stimulation with NMDARs and the associated NO release blocked, LTPL-VGCC was curtailed by inhibition of NO synthase or of the NO-receptor guanylyl cyclase to the same extent as occurred with inhibition of L-VGCCs. Unlike LTPNMDAR at these synapses, LTPL-VGCC was unaffected in mice lacking endothelial NO synthase, implying that the major source of the NO is neuronal. Transient delivery of exogenous NO paired with tetanic synaptic stimulation under conditions of NMDAR blockade resulted in a long-lasting potentiation that was sensitive to inhibition of NO-receptor guanylyl cyclase but was unaffected by inhibition of L-VGCCs. The results indicate that NO, acting through its second messenger cGMP, plays an unexpectedly important role in L-VGCC-dependent, NMDAR-independent LTP, possibly as a retrograde messenger generated in response to opening of postsynaptic L-VGCCs and/or as a signal acting postsynaptically, perhaps to facilitate changes in gene expression.
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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 Socratic graph.