Elsevier BV Acta Medica Okayama 0031-9384 261 2023 Oxytocin increased intragastric pressure in the forestomach of rats via the dorsal vagal complex 114087 EN Motoi Kobashi Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Science, Okayama University Yuichi Shimatani Department of Medical Engineering, Faculty of Engineering, Tokyo City University Masako Fujita Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Science, Okayama University We previously reported that appetite enhancing peptides facilitated phasic contractions of the distal stomach and relaxed the forestomach via the dorsal vagal complex (DVC). The present study investigated the effects of anorectic substances on gastric reservoir function. The effects of oxytocin on the motility of the forestomach were examined in rats anesthetized with urethane chloralose. Gastric motor responses were measured using an intragastric balloon. The fourth ventricular administration of oxytocin (0.1 1.0 nmol) increased intragastric pressure (IGP) in the forestomach in a dose dependent manner. Conversely, the administration of oxytocin (0.3 nmol) suppressed phasic contractions of the distal stomach. These responses were opposite to those of appetite enhancing peptides in previous studies. The oxytocin response in the forestomach was not observed after bilateral cervical vagotomy. The effects of oxytocin on forestomach motility were examined in animals that underwent ablation of the area postrema (AP) to clarify its involvement. Although the magnitude of the response to the fourth ventricular administration of oxytocin decreased, a significant response was still observed. A microinjection of oxytocin (3 pmol) into the AP, the left medial nucleus of the nucleus tractus solitarius (mNTS), the left commissural part of the NTS, or the left dorsal motor nucleus of the vagus was performed. The oxytocin injection into the AP and/or mNTS induced a rapid and large increase in IGP in the forestomach. Prior injection of L-368,899, an oxytocin receptor antagonist, into both the AP and mNTS attenuated the oxytocin response of the forestomach induced by fourth ventricular administration of oxytocin. These results indicate that oxytocin acts on the AP and/or mNTS to increase IGP in the forestomach via vagal preganglionic neurons. No potential conflict of interest relevant to this article was reported.

Elsevier Acta Medica Okayama 1566-0702 228 2020 Orexin A and B in the rat superior salivatory nucleus 102712 EN Tadasu Sato Division of Oral and Craniofacial Anatomy, Tohoku University Graduate School of Dentistry Takehiro Yajima Division of Oral and Craniofacial Anatomy, Tohoku University Graduate School of Dentistry Masako Fujita Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences Motoi Kobashi Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences Hiroyuki Ichikawa Division of Oral and Craniofacial Anatomy, Tohoku University Graduate School of Dentistry Ryusuke Yoshida Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences Yoshihiro Mitoh Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences Orexin (OX), which regulates sleep and wakefulness and feeding behaviors has 2 isoforms, orexin-A and -B (OXA and OXB). In this study, the distribution of OXA and OXB was examined in the rat superior salivatory nucleus (SSN) using retrograde tracing and immunohistochemical and methods. OXA- and OXB-immunoreactive (-ir) nerve fibers were seen throughout the SSN. These nerve fibers surrounded SSN neurons retrogradely labeled with Fast blue (FB) from the corda-lingual nerve. FB-positive neurons had pericellular OXA- (47.5%) and OXB-ir (49.0%) nerve fibers. Immunohistochemistry for OX receptors also demonstrated the presence of OX1R and OX2R in FB-positive SSN neurons. The majority of FB-positive SSN neurons contained OX1R- (69.7%) or OX2R-immunoreactivity (57.8%). These neurons had small and medium-sized cell bodies. In addition, half of FB-positive SSN neurons which were immunoreactive for OX1R (47.0%) and OX2R (52.2%) had pericellular OXA- and OXB-ir nerve fibers, respectively. Co-expression of OX1R- and OX2R was common in FB-positive SSN neurons. The present study suggests a possibility that OXs regulate the activity of SSN neurons through OX receptors. No potential conflict of interest relevant to this article was reported.

Elsevier Acta Medica Okayama 0304-3940 2020 Effects of Bitter Receptor Antagonists on Behavioral Lick Responses of Mice 135041 EN Michimasa Masamoto Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Yoshihiro Mitoh Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Motoi Kobashi Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Noriatsu Shigemura Section of Oral Neuroscience, Graduate School of Dental Sciences, Kyushu University Ryusuke Yoshida Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Bitter taste receptors TAS2Rs detect noxious compounds in the oral cavity. Recent heterologous expression studies reported that some compounds function as antagonists for human TAS2Rs. For examples, amino acid derivatives such as γ-aminobutyric acid (GABA) and Nα,Nα-bis(carboxymethyl)-L-Lysine (BCML) blocked responses to quinine mediated by human TAS2R4. Probenecid inhibited responses to phenylthiocarbamide mediated by human TAS2R38. In this study, we investigated the effects of these human bitter receptor antagonists on behavioral lick responses of mice to elucidate whether these compounds also function as bitter taste blockers. In short-term (10 s) lick tests, concentration-dependent lick responses to bitter compounds (quinine-HCl, denatonium and phenylthiourea) were not affected by the addition of GABA or BCML. Probenecid reduced aversive lick responses to denatonium and phenylthiourea but not to quinine-HCl. In addition, taste cell responses to phenylthiourea were inhibited by probenecid. These results suggest some bitter antagonists of human TAS2Rs can work for bitter sense of mouse. No potential conflict of interest relevant to this article was reported.

Acta Medica Okayama 1990 Convergence of Hepatic Osmoreceptive Inputs on Sodium-Responsive Units Within the Nucleus of the Solitary Tract of the Rat EN No potential conflict of interest relevant to this article was reported.