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Bradykinin (BK) and its receptors, B1and B2, in trigeminal ganglion (TG) neurons are involved in the regulation of pain. Recent studies have revealed that B1receptors are expressed in neonatal rat TG neurons; however, the intracellular signaling pathway following B1receptor activation remains to be elucidated. To investigate the mechanism by which B1receptor activation leads to intracellular Ca2+mobilization, we measured the intracellular free Ca2+concentration ([Ca2+]i) in primary-cultured TG neurons. The application of Lys-[Des-Arg9]BK (B1receptor agonist) increased the [Ca2+]iin these TG neurons even in the absence of extracellular Ca2+. Pretreatment with inhibitors of ryanodine receptors or sarco/endoplasmic reticulum Ca2+-ATPase suppressed the increase in Lys-[Des-Arg9]BK-induced [Ca2+]i. The Lys-[Des-Arg9]BK-induced [Ca2+]iincrease was unaffected by phospholipase-C inhibitor. B1receptor activation-induced [Ca2+]iincrease was suppressed by phosphodiesterase inhibitor and enhanced by adenylyl cyclase inhibitor. These results suggest that B1receptor activation suppresses intracellular cAMP production via adenylyl cyclase inhibition and mobilizes intracellular Ca2+via ryanodine receptors that access intracellular Ca2+stores.

Extracellular ATP, an essential pain mediator, is received by cell-surface ionotropic P2X andor metabotropic P2Y receptors. Although the contribution of P2X3andor P2X23receptors toward the pain mechanism is well described in trigeminal ganglion neurons, the expression of other subtypes of P2X receptor remains to be clarified. We examined expression of P2X receptor mRNA and measured intracellular free Ca2concentration (Ca2i) by the activation of these receptors by fura-2 fluorescence in primary cultured rat trigeminal ganglion neurons. Real-time reverse transcription-PCR analysis revealed mRNA expression of P2X receptor subtype P2X1, P2X3, and P2X4in trigeminal ganglion neurons. In the presence of extracellular Ca2, the application of P2X receptors agonists, ATP, ,-methylene ATP or ,-methylene ATP induced Ca2influx significantly. The ATP-induced increase in Ca2iwas inhibited by a series of selective antagonists for P2X1, P2X3, or P2X4receptors. These results indicate that trigeminal ganglion neurons functionally express P2X1, P2X3, and P2X4receptors and that these receptors are involved in the mediation of not only nociceptive but also neuropathic pain in the orofacial area.

Odontoblasts, well-polarized columnar cells at the periphery of the dental pulp, originate from neural crest cells. They are primarily involved in dentin formation (dentinogenesis) as sites of the synthesis and secretion of collagenous and non-collagenous matrix proteins, and also participate in the directional transport of Ca2+from the circulation to the dentin/mineralizing front. Dentinogenesis is activated by : 1) pulpal patho-physiological events, such as intra-pulpal inflammatory responses, physiological or developmental processes, and 2) events at the dentin surface, such as variousimechanical/heat/coldjstimuli applied to the tooth surface. Therefore, the aim of this communication is to give an overview of the Ca2+-signaling system, which may have a major role in dentin formation in both physiological and pathological settings. Special attention will be given to discussion of the following : 1) sequential Ca2+signaling pathways from internal inositol 1,4,5-trisphosphate (IP3) production viathe activation of phospholipase C-coupled receptors to the release of Ca2+from IP3-sensitive Ca2+stores, 2) subsequent Ca2+influx viastore-operated Ca2+channels, and 3) the expression of transient receptor potential channels coupled with Na+-Ca2+exchangers in odontoblasts.

Although the central role of ameloblasts in synthesis and resorption of enamel matrix proteins during amelogenesis is well documented, the Ca2+-transport/extrusion mechanism remains to be fully elucidated. To clarify Ca2+-transport in rat ameloblasts, we investigated expression and localization of Na+-Ca2+exchanger (NCX) isoforms and the functional characteristics of their ion transporting/pharmacological properties. RT-PCR and immunohistochemical analyses revealed expression of NCX1 and NCX3 in ameloblasts, localized in the apical membrane. In patch-clamp recordings, Ca2+efflux by Na+-Ca2+exchange showed dependence on external Na+. Ca2+influx by Na+-Ca2+exchange, measured by fura-2 fluorescence, showed dependence on extracellular Ca2+concentration, and it was blocked by NCX inhibitors KB-R7943, SEA0400, and SN-6. These results showed significant expression of NCX1 and NCX3 in ameloblasts, indicating their involvement in the directional Ca2+extrusion pathway from cells to the enamel mineralizing front.

Temporomandibular disorders are a group of chronic and painful conditions in the masticatory musculature and temporomandibular joint. The pathological mechanisms underlying temporomandibular disorders remain to be clarified; however, it is known that disturbances in neurophysiological, cognitive, behavioral and neuromuscular functions are involved in the development and persistence of such disorders. In addition, it has been suggested that neuropathological changes in the central nervous system are involved in the development of temporomandibular disorders. This review describes changes in the cortical machinery in patients with temporomandibular disorders by comparing neuromagnetic signals between healthy subjects and patients elicited by observing jaw opening movements made by another person.

ABSTRACTClear findings relative to where in the brain the starting point of voluntary swallowing is controlled were obtained in the present magnetoencephalographic study. Namely, the cerebral activity was observed in the cingulate gyrus and supplementary motor area for about 80 ms between 1,000 and 1,500 ms before swallowing in all test subjects. Thus, it is clear that this type of central control mechanism also plays an important role in complicated swallowing movements.