The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis(Vc) is the first relay site for the orofacial nociceptive inputs via the thin myelinatedAδ and unmyelinated C primary afferent fibers. Borneol, one of the valuable timehonoredherbal ingredients in traditional Chinese medicine, is a popular treatmentfor anxiety, anesthesia, and antinociception. However, to date, little is known asto how borneol acts on the SG neurons of the Vc. To close this gap, the whole-cellpatch-clamp technique was applied to elucidate the antinociceptive mechanismresponding for the actions of borneol on the SG neurons of the Vc in mice. In thevoltage-clamp mode, holding at –60 mV, the borneol-induced non-desensitizinginward currents were not affected by tetrodotoxin, a voltage-gated Na+ channelblocker, 6-cyano-7-nitro-quinoxaline-2,3-dione, a non-N-methyl-D-aspartate (NMDA)glutamate receptor antagonist and DL-2-amino-5-phosphonopentanoic acid, anNMDA receptor antagonist. However, borneol-induced inward currents were partiallydecreased in the presence of picrotoxin, a -aminobutyric acid (GABA)A receptorantagonist, or strychnine, a glycine receptor antagonist, and was almost suppressedin the presence of picrotoxin and strychnine. Though borneol did not show any effecton the glycine-induced inward currents, borneol enhanced GABA-mediatedresponses. Beside, borneol enhanced the GABA-induced hyperpolarization under thecurrent-clamp mode. Altogether, we suggest that borneol contributes in part towardmediating the inhibitory GABA and glycine transmission on the SG neurons of the Vcand may serve as an herbal therapeutic for orofacial pain ailments.

The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis(Vc) is the first relay site for the orofacial nociceptive inputs via the thin myelinatedAδ and unmyelinated C primary afferent fibers. Borneol, one of the valuable timehonoredherbal ingredients in traditional Chinese medicine, is a popular treatmentfor anxiety, anesthesia, and antinociception. However, to date, little is known asto how borneol acts on the SG neurons of the Vc. To close this gap, the whole-cellpatch-clamp technique was applied to elucidate the antinociceptive mechanismresponding for the actions of borneol on the SG neurons of the Vc in mice. In thevoltage-clamp mode, holding at –60 mV, the borneol-induced non-desensitizinginward currents were not affected by tetrodotoxin, a voltage-gated Na+ channelblocker, 6-cyano-7-nitro-quinoxaline-2,3-dione, a non-N-methyl-D-aspartate (NMDA)glutamate receptor antagonist and DL-2-amino-5-phosphonopentanoic acid, anNMDA receptor antagonist. However, borneol-induced inward currents were partiallydecreased in the presence of picrotoxin, a -aminobutyric acid (GABA)A receptorantagonist, or strychnine, a glycine receptor antagonist, and was almost suppressedin the presence of picrotoxin and strychnine. Though borneol did not show any effecton the glycine-induced inward currents, borneol enhanced GABA-mediatedresponses. Beside, borneol enhanced the GABA-induced hyperpolarization under thecurrent-clamp mode. Altogether, we suggest that borneol contributes in part towardmediating the inhibitory GABA and glycine transmission on the SG neurons of the Vcand may serve as an herbal therapeutic for orofacial pain ailments.