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 in | Neuroscience letters Vol. 468; no. 3; pp. 326 - 329 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Shannon
Elsevier Ireland Ltd
14.01.2010
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0304-3940 1872-7972 1872-7972 |
DOI: | 10.1016/j.neulet.2009.11.025 |