Abstract:
:Thymol, which is contained in thyme essential oil, has various actions including antinociception and nerve conduction inhibition. Although thymol activates transient receptor potential (TRP) channels expressed in heterologous cells, it remains to be examined whether this is so in native neurons. It has not yet been examined how thymol affects synaptic transmission. In order to know how thymol modulates excitatory transmission with a focus on TRP activation, we investigated its effect on glutamatergic spontaneous excitatory transmission in lamina II (substantia gelatinosa; SG) neurons with which nerve terminals expressing TRP channels make synaptic contacts. The experiment was performed by using the blind whole-cell patch-clamp technique in adult rat spinal cord slices. Superfusing thymol (1 mM) for 3 min reversibly increased the frequency of spontaneous excitatory postsynaptic current (sEPSC) with a minimal increase in its amplitude in all neurons examined. Seventy-seven% of the neurons produced an outward current at a holding potential of -70 mV. The sEPSC frequency increase and outward current produced by thymol were concentration-dependent with almost the same half-maximal effective concentration (EC50) values of 0.18 and 0.14 mM, respectively. These activities were repeated at a time interval of 30 min, although the sEPSC frequency increase but not outward current recovered with a slow time course. Voltage-gated Na(+)-channel blocker tetrodotoxin did not affect the thymol activities. The sEPSC frequency increase was inhibited by TRPA1 antagonist HC-030031 but not TRPV1 and TRPM8 antagonist (capsazepine and BCTC, respectively), while these antagonists had no effect on the outward current. This was so, albeit the two thymol activities had similar EC50 values. It is concluded that thymol increases the spontaneous release of L-glutamate onto SG neurons by activating TRPA1 channels while producing an outward current without TRP activation. Considering that the SG plays a pivotal role in modulating nociceptive transmission from the periphery, these actions of thymol could contribute to at least a part of its antinociceptive effect.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Xu ZH,Wang C,Fujita T,Jiang CY,Kumamoto Edoi
10.1016/j.neulet.2015.08.042subject
Has Abstractpub_date
2015-10-08 00:00:00pages
94-9eissn
0304-3940issn
1872-7972pii
S0304-3940(15)30112-9journal_volume
606pub_type
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