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Related Concept Videos

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

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Related Experiment Video

Updated: Jun 12, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Nitric oxide and neuronal death.

Guy C Brown1

  • 1Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, United Kingdom. gcb@mole.bio.cam.ac.uk

Nitric Oxide : Biology and Chemistry
|June 16, 2010
PubMed
Summary

Nitric oxide (NO) has dual effects on neurons. High NO levels can cause neuronal death through energy depletion or apoptosis, while low NO levels can protect neurons by blocking cell death pathways.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Nitric oxide (NO) plays a complex role in neuronal function and survival.
  • Its effects vary significantly depending on concentration and cellular context.

Purpose of the Study:

  • To elucidate the multifaceted mechanisms by which nitric oxide influences neuronal death and survival.
  • To differentiate the pathways involved in NO-induced necrosis, apoptosis, and neuroprotection.

Main Methods:

  • Review of existing literature on NO signaling pathways in neurons.
  • Analysis of molecular mechanisms including mitochondrial function, energy metabolism, and signal transduction pathways (e.g., MAPK, NF-kappaB).
  • Examination of the role of NO in excitotoxicity and inflammatory responses.

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Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds
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Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds

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Application of Genetically Encoded Fluorescent Nitric Oxide (NO&#8226;) Probes, the geNOps, for Real-time Imaging of NO&#8226; Signals in Single Cells
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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

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Last Updated: Jun 12, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds
08:23

Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds

Published on: February 16, 2022

Application of Genetically Encoded Fluorescent Nitric Oxide (NO&#8226;) Probes, the geNOps, for Real-time Imaging of NO&#8226; Signals in Single Cells
08:32

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

Main Results:

  • High NO levels induce necrosis via energy depletion (inhibiting respiration and glycolysis) or apoptosis through oxidant signaling.
  • Low NO levels can be neuroprotective by activating cGMP-dependent pathways or inhibiting mitochondrial permeability.
  • NO can also protect by modulating inflammatory responses and protein S-nitrosylation.

Conclusions:

  • Nitric oxide exhibits a concentration-dependent dual role in neuronal fate, capable of inducing both death and protection.
  • Understanding these complex pathways is crucial for developing therapeutic strategies targeting neurodegenerative diseases.