Kentaro Ono

After university graduation at 1999 until 2016, I have studied body fluid homeostasis, involving central sensory neurons in the circumventricular organs lacking the blood-brain barrier under direction of Prof. Inenaga in Kyushu Dental University. In a series of the study, I and colleagues revealed neuronal circuits, chemical signaling, channel mechanism by electrophysiology (whole-cell patch-clamp recordings and multi-array extracellular recordings) using brain slices or dissociated neurons, behavioral observation (drinking), RT-PCR and immunofluorescent techniques. I had experienced two collaborations with other laboratories (National Institute for Basic Biology and Saga University). In the former collaboration for an extracellular sodium-sensitive sodium channel, Nax, I succeeded to record ionic current via opening of the channel in dissociated dorsal root ganglion neurons (the study was published in Nature Neuroscience). Additionally, I have studied salivary functions in humans and experimental animals. In animal studies, we revealed availability of cholinergic agonists as sialogogues for xerostomia and its side effects in central and peripheral system. In human studies, we investigated salivary secretion in healthy humans and xerostomia patients with developments of new evaluation methods using MRI with clinical researchers. Since 2007, I have studied pain research, independently. I and colleagues succeeded cell classification of trigeminal ganglion neurons into some functionally-homogenous subgroups, and showed that there were some differences in algesic properties of a few subgroups between the trigeminal and dorsal root ganglions, or between rats and mice. In our developed facial cancer model, we demonstrated that cancer-induced pain hypersensitivity is caused by central glial activation, independent of inflammation and nerve injury. For one and half year from 2012, I worked in Bluestone Center, New York University (Prof. Brian L. Schmidt’s lab), and further studied cancer-induced pain and pigmentation-dependent nociception. In collaboration with National Cancer Center Japan, I and colleagues newly developed nociception evaluation systems for intraoral pain in conscious rats at 2015. By using the methods, we revealed patho-physiological mechanisms underlying oral ulcer-induced pain. In collaboration with Tsumura (Kampo medicine company), we identified active analgesic ingredients in a herbal medicine for oral ulcer. Currently, I have studied pain mechanism in some dental diseases and tactile mechanism in the orofacial region, based on my past experiences.