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Histamine receptors are densely expressed in the mesencephalic trigeminal nucleus (MesV) and trigeminal motor nucleus. However, little is known about the functional roles of neuronal histamine in controlling oral-motor activity. Thus, using the whole-cell recording technique in brainstem slice preparations from Wistar rats aged between postnatal days 7 and 13, we investigated the effects of histamine on the MesV neurons innervating the masseter muscle spindles and masseter motoneurons (MMNs) that form a reflex arc for the jaw-closing reflex. Bath application of histamine (100 μM) induced membrane depolarization in both MesV neurons and MMNs in the presence of tetrodotoxin, whereas histamine decreased and increased the input resistance in MesV neurons and MMNs, respectively. The effects of histamine on MesV neurons and MMNs were mimicked by an H1 receptor agonist, 2-pyridylethylamine (100 μM). The effects of an H2 receptor agonist, dimaprit (100 μM), on MesV neurons were inconsistent, whereas MMNs were depolarized without changes in the input resistance. An H3 receptor agonist, immethridine (100 μM), also depolarized both MesV neurons and MMNs without changing the input resistance. Histamine reduced the peak amplitude of postsynaptic currents (PSCs) in MMNs evoked by stimulation of the trigeminal motor nerve (5N), which was mimicked by 2-pyridylethylamine but not by dimaprit or immethridine. Moreover, 2-pyridylethylamine increased the failure rate of PSCs evoked by minimal stimulation and the paired-pulse ratio. These results suggest that histaminergic inputs to MesV neurons through H1 receptors are involved in the suppression of the jaw-closing reflex although histamine depolarizes MesV neurons and/or MMNs.

The aim of regenerative medicine is to restore the original functions of tissues and organs damaged by disease or impairment. Stem cell transfusion has been used clinically as regenerative therapy in a wide range of fields. This therapy promotes regeneration of partially damaged tissues or organs by transfer of tissue stem cells. Teeth are produced from dental germ, which is induced by interactions between epithelial and mesenchymal stem cells. Wnt signals are heavily involved in this process. Furthermore, it has been shown that β-catenin is expressed in the nucleus of odontoblasts and dentinal cells located immediately under repaired dentine after pulpotomy, and that macrophages in dental pulp express Wnt10a, suggesting involvement of Wnt10a in odontoblasts in generation and repair processes. However, little is known about the involvement of Wnt10a in odontoblasts in regenerated pulp tissues. Hayashi et al. transplanted dental pulp, bone marrow, adipose stem cells, or culture supernatants derived from each of them in the ectopic tooth transplantation. As a result, we have succeeded in regenerating dental pulp tissue that expresses the dental pulp marker TRH-DE, regardless of the transplantation. In this study, we used this model to examine morphologically how Wnt10a and odontoblasts change with time in regenerated dental pulp. We then analyzed the dynamics of Wnt10a in dentinal induction in dental pulp stem cells. The results of this study showed an increase in odontoblasts with increased regeneration of dental pulp, and these odontoblasts expressed Wn-t10a. Expression of DSPP increases upon inhibition of expression of DKK1, and induction of dentinal differentiation occurs via expression of Wnt10a in dental pulp regeneration. Therefore, Wnt10a is a candidate as a non-cellular agent for induction of dental pulp regeneration with dentine-inducing capacity.

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