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Related Experiment Video

Updated: May 14, 2026

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

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Published on: March 16, 2017

The relation of different-scale membrane processes under nitric oxide influence.

Nadiya A Brazhe Ulyanova¹, Liudmila A Erokhova, Anatolii A Churin

¹Department of Biophysics, Biological Faculty, Moscow State University, Leninskie gory, 1/12, Moscow, Russia 119992.

Journal of Biological Physics

|January 25, 2013

Summary

Nitric oxide (NO) activates potassium channels, reducing calcium levels and membrane viscosity in neurons. This impacts neuron activity and signal transmission through physical property changes.

Keywords:

membrane processes neuron nitric oxide redistribution of calcium

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Analytical Techniques for Assaying Nitric Oxide Bioactivity

Analytical Techniques for Assaying Nitric Oxide Bioactivity

Published on: June 18, 2012

Area of Science:

Neuroscience
Cellular Biology
Biophysics

Background:

Neuron activity, including rhythmic firing, synaptic transmission, and excitation propagation, relies on cellular-level processes.
Modulation of neuronal function is intrinsically linked to alterations in plasma membrane and organelle properties.

Purpose of the Study:

To investigate the effects of nitric oxide (NO) on ion channel activity, specifically voltage-dependent potassium channels (K(V)).
To examine the relationship between NO, membrane microviscosity, and intracellular calcium (Ca(2+)) levels.
To determine NO's influence on the refractive index of neurons and its potential implications for cellular structure.

Main Methods:

Electrophysiological recordings to assess ion channel activity.
Fluorescent probes or other biophysical techniques to measure membrane microviscosity.
Calcium imaging or quantification methods to determine bound and stored Ca(2+) levels.
Optical measurements to evaluate changes in neuronal refractive index.

Main Results:

Nitric oxide (NO) was found to activate voltage-dependent potassium channels (K(V)).
NO significantly decreased the amount of both membrane-bound and intracellularly stored calcium (Ca(2+)).
A reduction in the microviscosity of cytosomal membranes and an alteration in the refractive index of neurons were observed following NO application.

Conclusions:

NO-induced activation of K(V) channels and subsequent decrease in Ca(2+) influence neuronal excitability.
Changes in membrane microviscosity and refractive index suggest NO alters neuronal plasma membrane physicochemical properties.
NO-mediated structural reorganization within the cytoplasm, including vesicle dynamics and cytoskeleton rearrangement, may contribute to altered signal transmission.