Intranasal Chemosensory Lateralization Through the Multi-electrode Transcutaneous Electrical Nasal Bridge Stimulation

Numerous studies have been conducted on display techniques for intranasal chemosensory perception. However, a limited number of studies have focused on the presentation of sensory spatial information. To artificially produce intranasal chemosensory spatial perception, we focused on a technique to induce intranasal chemosensation by transcutaneous electrical stimulation between the nasal bridge and the back of the neck. Whether this technique stimulates the trigeminal nerve or the olfactory nerve remains debatable; if this method stimulates the trigeminal nerve, the differences in the amount of stimulation to the left and right trigeminal branches would evoke lateralization of intranasal chemosensory perception. Therefore, we propose a novel method to lateralize intranasal chemosensation by selectively stimulating the left or right trigeminal nerve branches through the shifting of an electrode on the nasal bridge to the left or right. Finite element simulations reveal that electrical stimulation applied between the electrodes on the left/right nasal bridge and the back of the neck results in the construction of a high current density area on the left/right branch of the trigeminal nerve. The results of two psychophysical experiments reveal that intranasal chemosensation can be lateralized by using the proposed method. The results of our experiment also suggest that lateralization is not the result of electrically induced tactile sensation of the skin surface but rather due to the distribution of stimuli to the trigeminal nerves. To the best of our knowledge, this study is the first successful lateralization of intranasal chemosensation that utilizes an easy-to-apply method without involving nostril blocking

Rho Kinase, Myosin-II, and p42/44 MAPK Control Extracellular Matrix-mediated Apical Bile Canalicular Lumen Morphogenesis in HepG2 Cells

The molecular mechanisms that regulate multicellular architecture and the development of extended apical bile canalicular lumens in hepatocytes are poorly understood. Here, we show that hepatic HepG2 cells cultured on glass coverslips first develop intercellular apical lumens typically formed by a pair of cells. Prolonged cell culture results in extensive organizational changes, including cell clustering, multilayering, and apical lumen morphogenesis. The latter includes the development of large acinar structures and subsequent elongated canalicular lumens that span multiple cells. These morphological changes closely resemble the early organizational pattern during development, regeneration, and neoplasia of the liver and are rapidly induced when cells are cultured on predeposited extracellular matrix (ECM). Inhibition of Rho kinase or its target myosin-II ATPase in cells cultured on glass coverslips mimics the morphogenic response to ECM. Consistently, stimulation of Rho kinase and subsequent myosin-II ATPase activity by lipoxygenase-controlled eicosatetranoic acid metabolism inhibits ECM-mediated cell multilayering and apical lumen morphogenesis but not initial apical lumen formation. Furthermore, apical lumen remodeling but not cell multilayering requires basal p42/44 MAPK activity. Together, the data suggest a role for hepatocyte-derived ECM in the spatial organization of hepatocytes and apical lumen morphogenesis and identify Rho kinase, myosin-II, and MAPK as potentially important players in different aspects of bile canalicular lumen morphogenesis