Expression of transient receptor potential vanilloid 1 and anoctamin 1 in rat trigeminal ganglion neurons innervating the tongue

2014 ◽  
Vol 106 ◽  
pp. 17-20 ◽  
Author(s):  
Takuya Kanazawa ◽  
Shigeji Matsumoto
Keyword(s):  
Trigeminal Ganglion ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Anoctamin 1 ◽  
Trigeminal Ganglion Neurons ◽  
Transient Receptor ◽  
Ganglion Neurons

scholarly journals Eugenol Inhibits K+ Currents in Trigeminal Ganglion Neurons

2007 ◽  
Vol 86 (9) ◽  
pp. 898-902 ◽  
Author(s):  
H.Y. Li ◽  
C.-K. Park ◽  
S.J. Jung ◽  
S.-Y. Choi ◽  
S.J. Lee ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Inhibitory Effects ◽  
Independent Manner ◽  
Voltage Gated ◽  
Trigeminal Ganglion Neurons ◽  
Transient Receptor ◽  
Ganglion Neurons

Eugenol, a natural capsaicin congener, is widely used in dentistry. Eugenol inhibits voltage-activated Na+ and Ca2+ channels in a transient receptor potential vanilloid 1 (TRPV1)-independent manner. We hypothesized that eugenol also inhibits voltage-gated K+ currents, and investigated this in rat trigeminal ganglion neurons and in a heterologous system using whole-cell patch clamping. Eugenol inhibited voltage-gated K+ currents, and the inhibitory effects of eugenol were observed in both capsaicin-sensitive and capsaicin-insensitive neurons. Pre-treatment with capsazepine, a well-known antagonist of TRPV1, failed to block the inhibitory effects of eugenol on K+ currents, suggesting no involvement of TRPV1. Eugenol inhibited human Kv1.5 currents stably expressed in Ltk− cells, where TRPV1 is not endogenously expressed. We conclude that eugenol inhibits voltage-gated K+ currents in a TRPV1-independent manner. The inhibition of voltage-gated K+ currents is likely to contribute to the irritable action of eugenol. Abbreviations: human Kv1.5 channel, hKv1.5; transient receptor potential vanilloid 1, TRPV1.

scholarly journals Transient Receptor Potential Channels Encode Volatile Chemicals Sensed by Rat Trigeminal Ganglion Neurons

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77998 ◽  
Author(s):  
Matthias Lübbert ◽  
Jessica Kyereme ◽  
Nicole Schöbel ◽  
Leopoldo Beltrán ◽  
Christian Horst Wetzel ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Volatile Chemicals ◽  
Trigeminal Ganglion Neurons ◽  
Potential Channels ◽  
Transient Receptor ◽  
Ganglion Neurons

scholarly journals Sumatriptan activates TRPA1

2019 ◽  
Vol 2 ◽  
pp. 251581631984715
Author(s):  
Alexandru Babes ◽  
Cristian Neacsu ◽  
Michael JM Fischer ◽  
Karl Messlinger
Keyword(s):  
Side Effects ◽  
Trigeminal Ganglion ◽  
Transient Receptor Potential ◽  
Animal Experiments ◽  
Receptor Potential ◽  
Membrane Currents ◽  
Nociceptive Neurons ◽  
Trigeminal Ganglion Neurons ◽  
Transient Receptor ◽  
Ganglion Neurons

Background: Migraine therapy with sumatriptan may cause adverse side effects like pain at the injection site, muscle pain, and transient aggravation of headaches. In animal experiments, sumatriptan excited or sensitized slowly conducting meningeal afferents. We hypothesized that sumatriptan may activate transduction channels of the “irritant receptor,” the transient receptor potential ankyrin type (TRPA1) expressed in nociceptive neurons. Methods: Calcium microfluorometry was performed in HEK293t cells transfected with human TRPA1 (hTRPA1) or a mutated channel (TRPA1-3C) and in dissociated trigeminal ganglion neurons. Membrane currents were recorded in the whole-cell patch clamp configuration. Results: Sumatriptan (10 and 400 µM) evoked calcium transients in hTRPA1-expressing HEK293t cells also activated by the TRPA1 agonist carvacrol (100 µM). In TRPA1-3C-expressing HEK293t cells, sumatriptan had hardly any effect. In rat trigeminal ganglion neurons, sumatriptan, carvacrol, and the transient receptor potential vanillod type 1 agonist capsaicin (1 µM) generated robust calcium signals. All sumatriptan-sensitive neurons (8% of the sample) were also activated by carvacrol (14%) and capsaicin (48%). In HEK293-hTRPA1 cells, sumatriptan (100 µM) evoked outwardly rectifying currents, which were almost completely inhibited by the TRPA1 antagonist HC-030031 (10 µM). Conclusion: Sumatriptan activates TRPA1 channels inducing calcium inflow and membrane currents. TRPA1-dependent activation of primary afferents may explain the painful side effects of sumatriptan.

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