Gabapentin Attenuates the Activation of Transient Receptor Potential A1 by Cinnamaldehyde.
- Author:
Sangsu BANG
1
;
Sungjae YOO
;
Sun Wook HWANG
Author Information
- Publication Type:Original Article
- Keywords: gabapentin; TRPA1; trigeminal ganglia; pain; CHO-K1
- MeSH: Acrolein; Amines; Animals; Cell Line; Cyclohexanecarboxylic Acids; gamma-Aminobutyric Acid; Ion Channels; Mice; Neurons; Sensory Receptor Cells; Trigeminal Ganglion
- From:Experimental Neurobiology 2009;18(1):1-7
- CountryRepublic of Korea
- Language:English
- Abstract: Gabapentin is used as an effective drug for relieving pain, but the main mechanism is still unclear. Recently, voltage-gated Ca2+ channel subunits are suggested for the main target for the analgesic action of gabapentin. We wonder whether gabapentin directly modulates other specific ion channels peripherally expressed in the sensory neurons. To test this, we used a heterologous expression system in which the cell lines transiently expressed thermosensitive transient receptor potential ion channels (thermoTRPs) as well as the primary cultured mouse trigeminal neurons. The application of gabapentin reduced the increases in the intracellular Ca2+ level caused by TRPA1 activation in the heterologous expression system whereas the responses via actions of other thermoTRPs were not dramatically affected by the gabapentin treatment. Gabapentin also attenuated the TRPA1-mediated intracellular Ca2+ increases in the cultured trigeminal neurons. These findings suggest TRPA1 in the peripheral sensory neurons as a novel target for the analgesic of gabapentin.
