Actions of ethanolamine on cultured sensory neurones from neonatal rats

Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones....

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Published inNeuroscience letters Vol. 468; no. 3; pp. 326 - 329
Main Authors Khairy, Hesham, Adjei, Gloria, Allen-Redpath, Keith, Scott, Roderick H.
Format Journal Article
LanguageEnglish
Published Shannon Elsevier Ireland Ltd 14.01.2010
Elsevier
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ISSN0304-3940
1872-7972
1872-7972
DOI10.1016/j.neulet.2009.11.025

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Abstract Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones. Ethanolamine is a product of metabolism of acylethanolamines including anandamide. In this study whole cell patch clamp recording and fura-2 Ca 2+ imaging techniques were used to characterize its actions on neonatal rat cultured dorsal root ganglion neurones. Ethanolamine (1 μM) increased the mean Ca 2+ transient produced by 1 mM caffeine and modulated Ca 2+ transients evoked by 60 mM KCl. Thapsigargicin (500 nM) inhibited the ethanolamine-evoked enhancement of Ca 2+ transients evoked by depolarisation. Voltage-activated K + currents were evoked from a holding potential of −70 mV by voltage step commands to 0 mV. Acute application of 1 μM ethanolamine produced irreversible current modulation. However, application of 100 nM ethanolamine reversibly increased or decreased K + currents. These effects of ethanolamine on voltage-activated K + currents were not sensitive to continual application of thapsigargicin. When applied alone thapsigargicin (500 nM) had no action on the mean K + current. In conclusion, ethanolamine may play distinct roles in the modulation of sensory neurone excitability by acting via different mechanisms to modulate K + channels and a component of intracellular Ca 2+ signalling. These data suggest that in a therapeutic context it may be difficult to predict the consequences of manipulating anandamide levels.
AbstractList Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones. Ethanolamine is a product of metabolism of acylethanolamines including anandamide. In this study whole cell patch clamp recording and fura-2 Ca(2+) imaging techniques were used to characterize its actions on neonatal rat cultured dorsal root ganglion neurones. Ethanolamine (1muM) increased the mean Ca(2+) transient produced by 1mM caffeine and modulated Ca(2+) transients evoked by 60mM KCl. Thapsigargicin (500nM) inhibited the ethanolamine-evoked enhancement of Ca(2+) transients evoked by depolarisation. Voltage-activated K(+) currents were evoked from a holding potential of -70mV by voltage step commands to 0mV. Acute application of 1muM ethanolamine produced irreversible current modulation. However, application of 100nM ethanolamine reversibly increased or decreased K(+) currents. These effects of ethanolamine on voltage-activated K(+) currents were not sensitive to continual application of thapsigargicin. When applied alone thapsigargicin (500nM) had no action on the mean K(+) current. In conclusion, ethanolamine may play distinct roles in the modulation of sensory neurone excitability by acting via different mechanisms to modulate K(+) channels and a component of intracellular Ca(2+) signalling. These data suggest that in a therapeutic context it may be difficult to predict the consequences of manipulating anandamide levels.Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones. Ethanolamine is a product of metabolism of acylethanolamines including anandamide. In this study whole cell patch clamp recording and fura-2 Ca(2+) imaging techniques were used to characterize its actions on neonatal rat cultured dorsal root ganglion neurones. Ethanolamine (1muM) increased the mean Ca(2+) transient produced by 1mM caffeine and modulated Ca(2+) transients evoked by 60mM KCl. Thapsigargicin (500nM) inhibited the ethanolamine-evoked enhancement of Ca(2+) transients evoked by depolarisation. Voltage-activated K(+) currents were evoked from a holding potential of -70mV by voltage step commands to 0mV. Acute application of 1muM ethanolamine produced irreversible current modulation. However, application of 100nM ethanolamine reversibly increased or decreased K(+) currents. These effects of ethanolamine on voltage-activated K(+) currents were not sensitive to continual application of thapsigargicin. When applied alone thapsigargicin (500nM) had no action on the mean K(+) current. In conclusion, ethanolamine may play distinct roles in the modulation of sensory neurone excitability by acting via different mechanisms to modulate K(+) channels and a component of intracellular Ca(2+) signalling. These data suggest that in a therapeutic context it may be difficult to predict the consequences of manipulating anandamide levels.
Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones. Ethanolamine is a product of metabolism of acylethanolamines including anandamide. In this study whole cell patch clamp recording and fura-2 Ca 2+ imaging techniques were used to characterize its actions on neonatal rat cultured dorsal root ganglion neurones. Ethanolamine (1 μM) increased the mean Ca 2+ transient produced by 1 mM caffeine and modulated Ca 2+ transients evoked by 60 mM KCl. Thapsigargicin (500 nM) inhibited the ethanolamine-evoked enhancement of Ca 2+ transients evoked by depolarisation. Voltage-activated K + currents were evoked from a holding potential of −70 mV by voltage step commands to 0 mV. Acute application of 1 μM ethanolamine produced irreversible current modulation. However, application of 100 nM ethanolamine reversibly increased or decreased K + currents. These effects of ethanolamine on voltage-activated K + currents were not sensitive to continual application of thapsigargicin. When applied alone thapsigargicin (500 nM) had no action on the mean K + current. In conclusion, ethanolamine may play distinct roles in the modulation of sensory neurone excitability by acting via different mechanisms to modulate K + channels and a component of intracellular Ca 2+ signalling. These data suggest that in a therapeutic context it may be difficult to predict the consequences of manipulating anandamide levels.
Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones. Ethanolamine is a product of metabolism of acylethanolamines including anandamide. In this study whole cell patch clamp recording and fura-2 Ca(2+) imaging techniques were used to characterize its actions on neonatal rat cultured dorsal root ganglion neurones. Ethanolamine (1muM) increased the mean Ca(2+) transient produced by 1mM caffeine and modulated Ca(2+) transients evoked by 60mM KCl. Thapsigargicin (500nM) inhibited the ethanolamine-evoked enhancement of Ca(2+) transients evoked by depolarisation. Voltage-activated K(+) currents were evoked from a holding potential of -70mV by voltage step commands to 0mV. Acute application of 1muM ethanolamine produced irreversible current modulation. However, application of 100nM ethanolamine reversibly increased or decreased K(+) currents. These effects of ethanolamine on voltage-activated K(+) currents were not sensitive to continual application of thapsigargicin. When applied alone thapsigargicin (500nM) had no action on the mean K(+) current. In conclusion, ethanolamine may play distinct roles in the modulation of sensory neurone excitability by acting via different mechanisms to modulate K(+) channels and a component of intracellular Ca(2+) signalling. These data suggest that in a therapeutic context it may be difficult to predict the consequences of manipulating anandamide levels.
Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels. However, the products of anandamide metabolism by fatty acid amide hydroxylase may also contribute to the altered excitability of sensory neurones. Ethanolamine is a product of metabolism of acylethanolamines including anandamide. In this study whole cell patch clamp recording and fura-2 Ca super(2+) imaging techniques were used to characterize its actions on neonatal rat cultured dorsal root ganglion neurones. Ethanolamine (1 kM) increased the mean Ca super(2+) transient produced by 1 mM caffeine and modulated Ca super(2+) transients evoked by 60 mM KCl. Thapsigargicin (500 nM) inhibited the ethanolamine-evoked enhancement of Ca super(2+) transients evoked by depolarisation. Voltage-activated K super(+) currents were evoked from a holding potential of -70 mV by voltage step commands to 0 mV. Acute application of 1 kM ethanolamine produced irreversible current modulation. However, application of 100 nM ethanolamine reversibly increased or decreased K super(+) currents. These effects of ethanolamine on voltage-activated K super(+) currents were not sensitive to continual application of thapsigargicin. When applied alone thapsigargicin (500 nM) had no action on the mean K super(+) current. In conclusion, ethanolamine may play distinct roles in the modulation of sensory neurone excitability by acting via different mechanisms to modulate K super(+) channels and a component of intracellular Ca super(2+) signalling. These data suggest that in a therapeutic context it may be difficult to predict the consequences of manipulating anandamide levels.
Author Adjei, Gloria
Allen-Redpath, Keith
Scott, Roderick H.
Khairy, Hesham
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Issue 3
Keywords Intracellular calcium stores
Voltage-activated potassium currents
Dorsal root ganglion
Endocannabinoids
Thapsigargicin
Spinal cord
Calcium
Rat
Rodentia
Central nervous system
Ionic current
Cannabinoid
Vertebrata
Mammalia
Endocannabinoid
Animal
Spinal ganglion
Intracellular
Potassium
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Snippet Some of the analgesic and antinociceptive properties of the endocannabinoid anandamide can be explained by modulation of voltage-activated ion channels....
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SubjectTerms Animals
Animals, Newborn
Biological and medical sciences
Calcium Signaling
Cells, Cultured
Dorsal root ganglion
Endocannabinoids
Ethanolamine - metabolism
Ethanolamine - pharmacology
Fundamental and applied biological sciences. Psychology
Ganglia, Spinal - cytology
Intracellular calcium stores
Patch-Clamp Techniques
Potassium Channels, Voltage-Gated - physiology
Potassium Chloride - pharmacology
Rats
Sensory Receptor Cells - drug effects
Sensory Receptor Cells - physiology
Thapsigargicin
Vertebrates: nervous system and sense organs
Voltage-activated potassium currents
Title Actions of ethanolamine on cultured sensory neurones from neonatal rats
URI https://dx.doi.org/10.1016/j.neulet.2009.11.025
https://www.ncbi.nlm.nih.gov/pubmed/19914344
https://www.proquest.com/docview/21444868
https://www.proquest.com/docview/733853312
Volume 468
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