Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Society  

We previously demonstrated that accurate regulation of isometric contraction (IC) of jaw-closing muscles to counteract the ramp load applied to the jaw in the jaw-opening direction is achieved through the calibration between the two sensations arising from muscle spindles (MSs) and periodontal mechanoreceptors (PMRs). However, it remains unclear whether this calibration mechanism accurately works at any jaw positions, i.e., any vertical dimensions of occlusion (VDO). In the present study, we examined the effects of altering VDO on the IC of the masseter muscles in complete dentulous and edentulous subjects. At a VDO higher than the original VDO (O-VDO), the root mean square (RMS) of masseter EMG activity increased more steeply with a load increase, resulting in an over-counteraction. The regression coefficient of the Load-RMS relationship significantly increased as the VDO was increased, suggesting that the overestimation became more pronounced with the VDO increases. Consistently also in the edentulous subjects, at a higher VDO than the O-VDO, a steeper increase in the RMS emerged with a delay in response to the same ramp load while a similar steeper increase was seen surprisingly even at a lower VDO. Thus, the edentulous subjects displayed a delayed overestimation of the ramp load presumably due to less and slowly sensitive mucous membrane mechanoreceptor (MMR) in alveolar ridge compared to the PMR. Taken together, the accurate calibration between the two sensations arising from MSs and PMRs/MMRs can be done only at the O-VDO, suggesting that the O-VDO is the best calibration point for performing accurate IC.

DOI： 10.1152/jn.00301.2022

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PubMed

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：MDPI AG  

Somatic expressions of either heteromeric TASK1/3 or homomeric TASK1/1 channels have been reported in various neurons, while expression of homomeric TASK3/3 channels has been re-ported only in dendrites. However, it is not known why homomeric TASK3/3 channels are hardly seen in somata of CNS neurons. Given the absence of somatic TASK3/3 channels, it should be clarified why dendritic expression of TASK3/3 channels is inevitable and necessary and how differentially distributed TASK1/1 and TASK3/3 channels play roles in soma-to-dendritic integration. Here, we addressed these questions. We found that TASK3-transfected HEK293 cells showed decreases in cell volume after being transferred from the cultured medium to HEPES Ringer, suggesting that expressions of TASK3 channels in cell bodies cause an osmolarity problem. Using TASK1- and TASK3-transfected oocytes, we also found that cGMP application slightly suppressed TASK3 currents while it largely enhanced TASK1 currents, alleviating the difference between TASK1 and TASK3 currents at physiological pH. As larger motoneurons have extensive dendritic trees while smaller motoneurons have poor ones, cGMP could integrate Ia-EPSPs to recruit small and large motoneurons synchronously by differentially modulating TASKI and TASK3 channels which were complementary distributed in soma and dendrites of motoneurons in the dorsolateral part of the trigeminal motor nucleus.

DOI： 10.3390/ijms24010344

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Frontiers Research Foundation  

Noradrenergic neurons in the locus coeruleus (LC) release noradrenaline (NA) that acts via volume transmission to activate extrasynaptic G-protein coupled receptors (GPCRs) in target cells throughout the brain. As the closest projection, the dorsal LC laterally adjoins the mesencephalic trigeminal nucleus (MTN), in which proprioceptive primary sensory neurons innervating muscle spindles of jaw-closing muscles are exceptionally located. MTN neurons express α2-adrenergic receptors (α2-ARs) and display hyperpolarization-activated cyclic nucleotide-gated (HCN) currents (Ihs), which is downregulated by α2-AR activation. To quantify the activity-dependent outcome of volume transmission of NA from LC to MTN, we investigated how direct LC activation inhibits Ih in MTN neurons by performing dual whole-cell recordings from LC and MTN neurons. Repetition of 20 Hz spike-train evoked with 1-s current-pulse in LC neurons every 30 s resulted in a gradual decrease in Ih evoked every 30 s, revealing a Hill-type relationship between the number of spike-trains in LC neurons and the degree of Ih inhibition in MTN neurons. On the other hand, when microstimulation was applied in LC every 30 s, an LC neuron repeatedly displayed a transient higher-frequency firing followed by a tonic firing at 5-10 Hz for 30 s. This subsequently caused a similar Hill-type inhibition of Ih in the simultaneously recorded MTN neuron, but with a smaller Hill coefficient, suggesting a lower signal transduction efficacy. In contrast, 20 Hz activity induced by a 1-s pulse applied every 5-10 s caused only a transient facilitation of Ih inhibition followed by a forced termination of Ih inhibition. Thus, the three modes of LC activities modulated the volume transmission to activate alpha2-adrenergic GPCR to differentially inhibit Ih in MTN neurons.

DOI： 10.3389/fncel.2022.841239

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Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1007/s00441-021-03452-5

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PubMed

Language：English   Publisher：南九州歯学会  

【目的】本研究は,成マウスの味蕾で特異的に発現する線維芽細胞増殖因子(Fgf)とその受容体(Fgfr)を見いだし,発現パターンを明らかにすることを目的とした.【方法】2つの舌上皮領域:1)味蕾を含む味覚上皮として有郭・葉状乳頭,2)味蕾を含まない非味覚上皮として舌中央部からトータルRNAを抽出した.全てのFgfとFgfrファミリー分子のRT-PCRを行って味覚上皮と非味覚上皮の間で比較し,味覚上皮で強く発現する分子を明らかにした.さらに,有郭乳頭の凍結切片でin situハイブリダイゼーションを行い、味蕾付近の発現パターンを解析した.in situハイブリダーゼーションと同時に,Kcnq1の免疫組織化学を行って味蕾の輪郭を可視化し,Fgfの発現が味蕾の内部であるか外側であるかを判別した.【結果】RT-PCRにより,22種のFgfのうちFgf1,9,13,14,20が,非味覚上皮よりも味覚上皮に強く発現することが示された.in situハイブリダイゼーションにより,Fgf1,13,14は味蕾に関連した発現が明らかになった.Fgf1は,殆どすべての味蕾細胞と味蕾近傍に強く発現していた.Fgf13,14は,一部の味蕾細胞に強く発現していた.一方,Fgf9,20は舌上皮に広く発現していた.【結論】Fgf1,13,14は味蕾に関連して発現しており,味蕾のホメオスタシスと機能に関与すると考えられる.(著者抄録)

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Basel  

It is known that desensitization of GABAA receptor (GABAAR)-mediated currents is paradoxically correlated with the slowdown of their deactivation, i.e., resensitization. It has been shown that an upregulation of calcineurin enhances the desensitization of GABAAR-mediated currents but paradoxically prolongs the decay phase of inhibitory postsynaptic currents/potentials without appreciable diminution of their amplitudes. The paradoxical correlation between desensitization and resensitization of GABAAR-mediated currents can be more clearly seen in response to a prolonged application of GABA to allow more desensitization, instead of brief pulse used in previous studies. Indeed, hump-like GABAAR currents were produced after a strong desensitization at the offset of a prolonged puff application of GABA in pyramidal cells of the barrel cortex, in which calcineurin activity was enhanced by deleting phospholipase C-related catalytically inactive proteins to enhance the desensitization/resensitization of GABAAR-mediated currents. Hump-like GABAAR currents were also evoked at the offset of propofol or barbiturate applications in hippocampal or sensory neurons, but not GABA applications. Propofol and barbiturate are useful to treat benzodiazepine/alcohol withdrawal syndrome, suggesting that regulatory mechanisms of desensitization/resensitization of GABAAR-mediated currents are important in understanding benzodiazepine/alcohol withdrawal syndrome. In this review, we will discuss the molecular and regulatory mechanisms underlying the desensitization and resensitization of GABAAR-mediated currents and their functional significances.

DOI： 10.3390/ijms21020563

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Frontiers Research Foundation  

Glutamatergic dendritic EPSPs evoked in cortical pyramidal neurons are depressed by activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels expressed in dendritic spines. This depression has been attributed to shunting effects of HCN current (Ih) on input resistance or Ih deactivation. Primary sensory neurons in the rat mesencephalic trigeminal nucleus (MTN) have the somata covered by spine-like microvilli that express HCN channels. In rat MTN neurons, we demonstrated that Ih enhancement apparently diminished the glutamate receptor (GluR) current (IGluR) evoked by puff application of glutamate/AMPA and enhanced a transient outward current following IGluR (OT-IGluR). This suggests that some outward current opposes inward IGluR. The IGluR inhibition displayed a U-shaped voltage-dependence with a minimal inhibition around the resting membrane potential, suggesting that simple shunting effects or deactivation of Ih cannot explain the U-shaped voltage-dependence. Confocal imaging of Na+ revealed that GluR activation caused an accumulation of Na+ in the microvilli, which can cause a negative shift of the reversal potential for Ih (Eh). Taken together, it was suggested that IGluR evoked in MTN neurons is opposed by a transient decrease or increase in standing inward or outward Ih, respectively, both of which can be caused by negative shifts of Eh, as consistent with the U-shaped voltage-dependence of the IGluR inhibition and the OT-IGluR generation. An electron-microscopic immunohistochemical study revealed the colocalization of HCN channels and glutamatergic synapses in microvilli of MTN neurons, which would provide a morphological basis for the functional interaction between HCN and GluR channels. Mathematical modeling eliminated the possibilities of the involvements of Ih deactivation and/or shunting effect and supported the negative shift of Eh which causes the U-shaped voltage-dependent inhibition of IGluR.

DOI： 10.3389/fncel.2018.00113

Other Link： https://www.frontiersin.org/articles/10.3389/fncel.2018.00113/full

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Frontiers Research Foundation  

The muscle contraction during voluntary movement is regulated by activities of α- and γ-motoneurons (αMNs and γMNs, respectively). The tension of jaw-closing muscles can be finely tuned over a wide range. This excellent function is likely to be achieved by the specific populations of αMNs innervating jaw-closing muscles. Indeed, we have recently demonstrated that in the rat dorsolateral trigeminal motor nucleus (dl-TMN), the size distribution of αMNs was bimodal and the population of smaller αMNs showed a size distribution similar to that of γMNs, by immunohistochemically identifying αMNs and γMNs based on the expressions of estrogen-related receptor gamma (Err3) and neuronal DNA binding protein NeuN together with ChAT. This finding suggests the presence of αMNs as small as γMNs. However, differences in the electrophysiological membrane properties between αMNs and γMNs remain unknown also in the dl-TMN. Therefore, in the present study, we studied the electrophysiological membrane properties of MNs in the dl-TMN of infant rats at postnatal days 7-12 together with their morphological properties using whole-cell current-clamp recordings followed by immunohistochemical staining with an anti-NeuN and anti-ChAT antibodies. We found that the ChAT-positive and NeuN-positive αMNs were divided into two subclasses: the first one had a larger cell body and displayed a 4-aminopyridine (4-AP)-sensitive current while the second one had a smaller cell body and displayed a less prominent 4-AP-sensitive current and a low-threshold spike, suitable for their orderly recruitment. We finally found that γMNs showing ChAT-positive and NeuN-negative immunoreactivities had smaller cell bodies and displayed an afterdepolarization mediated by flufenamate-sensitive cation current. It is suggested that these electrophysiological and morphological features of MNs in the dl-TMN are well correlated with the precise control of occlusion.

DOI： 10.3389/fncel.2018.00009

PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer-Verlag  

γ-motoneurons (γMNs) play a crucial role in regulating isometric muscle contraction. The slow jaw-closing during mastication is one of the most functional isometric contractions, which is developed by the rank-order recruitment of α-motoneurons (αMNs) in a manner that reflects the size distribution of αMNs. In a mouse spinal motor nucleus, there are two populations of small and large MNs; the former was identified as a population of γMNs based on the positive expression of the transcription factor estrogen-related receptor 3 (Err3) and negative expression of the neuronal DNA-binding protein NeuN, and the latter as that of αMNs based on the opposite pattern of immunoreactivity. However, the differential identification of αMNs and γMNs in the trigeminal motor nucleus (TMN) remains an assumption based on the size of cell bodies that were retrogradely stained with HRP. We here examined the size distributions of αMNs and γMNs in the dorsolateral TMN (dl-TMN) by performing immunohistochemistry using anti-Err3 and anti-NeuN antibodies. The dl-TMN was identified by immunopositivity for vesicular glutamate transporter-1. Immunostaining for choline acetyltransferase and Err3/NeuN revealed that the dl-TMN is composed of 65% αMNs and 35% γMNs. The size distribution of αMNs was bimodal, while that of γMNs was almost the same as that of the population of small αMNs, suggesting the presence of αMNs as small as γMNs. Consistent with the size concept of motor units, the presence of smaller jaw-closing αMNs was coherent with the inclusion of jaw-closing muscle fibers with smaller diameters compared to limb muscle fibers.

DOI： 10.1007/s00429-017-1400-8

PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Nature Publishing Group  

Anandamide (AEA) and N-oleoylethanolamine (OEA) are produced in the intestine and brain during fasting and satiety, respectively. Subsequently, AEA facilitates food intake via activation of cannabinoid type-1 receptors (CB1Rs) while OEA decreases food intake via activation of peroxisome proliferator-activated receptor-alpha (PPARalpha) and/or G-protein-coupled receptor 119 (GPR119). Neuronal activity in the gastrointestinal region of the autonomic insula (GI-Au-I) that rostrally adjoins the gustatory insula (Gu-I) increases during fasting, enhancing appetite while umami and sweet taste sensations in Gu-I enhances appetite in GI-Au-I, strongly suggesting the presence of a neural interaction between the Gu-I and GI-Au-I which changes depending on the concentrations of AEA and OEA. However, this possibility has never been investigated. In rat slice preparations, we demonstrate with voltage-sensitive dye imaging that activation of CB1Rs by AEA induces theta-rhythm oscillatory synchronization in the Gu-I which propagates into the GI-Au-I but stops at its caudal end, displaying an oscillatory coordination. The AEA-induced oscillation was abolished by a CB1R antagonist or OEA through activation of GPR119. Our results demonstrate that the neural coordination between the Gu-I and GI-Au-I is generated or suppressed by the opposing activities between CB1R and GPR119. This mechanism may be involved in the feeding behavior based on taste recognition.

DOI： 10.1038/srep32529

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Society for Neuroscience  

Because a rank-ordered recruitment of motor units occurs during isometric contraction of jaw-closing muscles, jaw-closing motoneurons (MNs) may be recruited in a manner dependent on their soma sizes or input resistances (IRs). In the dorsolateral part of the trigeminal motor nucleus (dl-TMN) in rats, MNs abundantly express TWIK (two-pore domain weak inwardly rectifying K channel)-related acid-sensitive-K⁺ channel (TASK)-1 and TASK3 channels, which determine the IR and resting membrane potential. Here we examined how TASK channels are involved in IR-dependent activation/recruitment of MNs in the rat dl-TMN by using multiple methods. The real-time PCR study revealed that single large MNs (>35 microm) expressed TASK1 and TASK3 mRNAs more abundantly compared with single small MNs (15-20 microm). The immunohistochemistry revealed that TASK1 and TASK3 channels were complementarily distributed in somata and dendrites of MNs, respectively. The density of TASK1 channels seemed to increase with a decrease in soma diameter while there were inverse relationships between the soma size of MNs and IR, resting membrane potential, or spike threshold. Dual whole-cell recordings obtained from smaller and larger MNs revealed that the recruitment of MNs depends on their IRs in response to repetitive stimulation of the presumed Ia afferents. 8-Bromoguanosine-cGMP decreased IRs in small MNs, while it hardly changed those in large MNs, and subsequently decreased the difference in spike-onset latency between the smaller and larger MNs, causing a synchronous activation of MNs. These results suggest that TASK channels play critical roles in rank-ordered recruitment of MNs in the dl-TMN.

DOI： 10.1523/ENEURO.0138-16.2016

PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Frontiers Research Foundation  

In a human fMRI study, it has been demonstrated that tasting and ingesting capsaicin activate the ventral part of the middle and posterior short gyri (M/PSG) of the insula which is known as the primary gustatory area, suggesting that capsaicin is recognized as a taste. Tasting and digesting spicy foods containing capsaicin induce various physiological responses such as perspiration from face, salivation, and facilitation of cardiovascular activity, which are thought to be caused through viscero-visceral autonomic reflexes. However, this does not necessarily exclude the possibility of the involvement of higher-order sensory-motor integration between the M/PSG and anterior short gyrus (ASG) known as the autonomic region of the insula. To reveal a possible functional coordination between the M/PSG and ASG, we here addressed whether capsaicin increases neural activity in the ASG as well as the M/PSG using fMRI and a custom-made taste delivery system. Twenty subjects participated in this study, and three tastant solutions: capsaicin, NaCl, and artificial saliva (AS) were used. Group analyses with the regions activated by capsaicin revealed significant activations in the bilateral ASG and M/PSG. The fMRI blood oxygenation level-dependent (BOLD) signals in response to capsaicin stimulation were significantly higher in ASG than in M/PSG regardless of the side. Concomitantly, capsaicin increased the fingertip temperature significantly. Although there was no significant correlation between the fingertip temperatures and BOLD signals in the ASG or M/PSG when the contrast [Capsaicin AS] or [Capsaicin NaCl] was computed, a significant correlation was found in the bilateral ASG when the contrast [2 x Capsaicin-NaCl-AS] was computed. In contrast, there was a significant correlation in the hypothalamus regardless of the contrasts. Furthermore, there was a significant correlation between M/PSG and ASG. These results indicate that capsaicin increases neural activity in the ASG as well as the M/PSG, suggesting that the neural coordination between the two cortical areas may be involved in autonomic responses to tasting spicy foods as reflected in fingertip temperature increases.

DOI： 10.3389/fnhum.2015.00720

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer  

We previously demonstrated that the deletion of phospholipase C-related catalytically inactive protein-1/2 (PRIP-1/2) enhances the desensitization of GABA_A receptors (GABA_ARs), while it facilitates their resensitization at the offset of GABA puff, causing a hump-like tail current (tail-I) in layer 3 (L3) pyramidal cells (PCs) of the barrel cortex. In the present study, we investigated whether inhibitory synaptic transmission in L3 PCs in the barrel cortex is altered in the PRIP-1/2 double-knockout (PRIP-DKO) mice, and if so, how the interaction between excitation and inhibition is subsequently modified. PRIP-1/2 deletion resulted in the prolongation of the decay phase of inhibitory postsynaptic currents/potentials (IPSCs/IPSPs) in L3 PCs evoked by stimulation of L3, leaving the overall features of miniature IPSCs unchanged. An optical imaging revealed that the spatiotemporal profile of a horizontal excitation spread across columns in L2/3 caused by L4 stimulation in the barrel cortex was more restricted in PRIP-DKO mice compared to the wild type, while those obtained in the presence of bicuculline were almost identical between the two genotypes. These findings suggest that PRIP-1/2 deletion enhances the lateral inhibition by prolonging inhibitory synaptic actions to limit the intercolumnar integration in the barrel cortex. Considering the present findings together with our previous study including a mathematical simulation, the prolongation of inhibitory synaptic actions is likely to result from an enhancement of desensitization followed by an enhanced resensitization in GABA_ARs.

DOI： 10.1007/s00424-014-1592-1

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Federation of European Neuroscience Societies  

The primary sensory neurons supplying muscle spindles of jaw-closing muscles are unique in that they have their somata in the mesencephalic trigeminal nucleus (MTN) in the brainstem, thereby receiving various synaptic inputs. MTN neurons display bursting upon activation of glutamatergic synaptic inputs while they faithfully relay respective impulses arising from peripheral sensory organs. The persistent sodium current (I_NaP) is reported to be responsible for both the generation of bursts and the relay of impulses. We addressed how I_NaP is controlled either to trigger bursts or to relay respective impulses as single spikes in MTN neurons. Protein kinase C (PKC) activation enhanced I_NaP only at low voltages. Spike generation was facilitated by PKC activation at membrane potentials more depolarized than the resting potential. By injection of a ramp current pulse, a burst of spikes was triggered from a depolarized membrane potential whereas its instantaneous spike frequency remained almost constant despite the ramp increases in the current intensity beyond the threshold. A puff application of glutamate preceding the ramp pulse lowered the threshold for evoking bursts by ramp pulses while chelerythrine abolished such effects of glutamate. Dihydroxyphenylglycine, an agonist of mGluR1/5, also caused similar effects, and increased both the frequency and impedance of membrane resonance. Immunohistochemistry revealed that glutamatergic synapses are made onto the stem axons, and that mGluR1/5 and Nav1.6 are co-localized in the stem axon. Taken together, glutamatergic synaptic inputs onto the stem axon may be able to switch the relaying to the bursting mode.

DOI： 10.1111/ejn.12858

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer  

Phospholipase C-related catalytically inactive proteins (PRIP-1/2) are previously reported to be involved in the membrane trafficking of GABA_A receptor (GABA_AR) and the regulation of intracellular Ca²⁺ stores. GABA_AR-mediated currents can be regulated by the intracellular Ca²⁺. However, in PRIP-1/2 double-knockout (PRIP-DKO) mice, it remains unclear whether the kinetic properties of GABA_ARs are modulated by the altered regulation of intracellular Ca²⁺ stores. Here, we investigated whether GABA_AR currents (I_GABA) evoked by GABA puff in layer 3 (L3) pyramidal cells (PCs) of the barrel cortex are altered in PRIP-DKO mice. The deletion of PRIP-1/2 enhanced the desensitization of I_GABA but induced a hump-like tail current (tail-I) at the GABA puff offset. I_GABA and the hump-like tail-I were suppressed by GABA_AR antagonists. The enhanced desensitization of I_GABA and the hump-like tail-I in PRIP-DKO PCs were mediated by increases in the intracellular Ca²⁺ concentration and were largely abolished by a calcineurin inhibitor and ruthenium red. Calcium imaging revealed that Ca²⁺-induced Ca²⁺ release (CICR) and subsequent store-operated Ca²⁺ entry (SOCE) are more potent in PRIP-DKO PCs than in wild-type PCs. A mathematical model revealed that a slowdown of GABA-unbinding rate and an acceleration of fast desensitization rate by enhancing its GABA concentration dependency are involved in the generation of hump-like tail-Is. These results suggest that in L3 PCs of the barrel cortex in PRIP-DKO mice, the increased calcineurin activity due to the potentiated CICR and SOCE enhances the desensitization of GABA_ARs and slows the GABA-unbinding rate, resulting in their unusual resensitization following removal of GABA.

DOI： 10.1007/s00424-014-1511-5

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer  

It has been reported that the 90-deg arm abduction force counteracting external adduction loads appeared to be smaller under teeth clenching condition than under non-clenching condition. To elucidate the physiological mechanism underlying the possible inhibitory effect of teeth clenching on the arm abduction, we have attempted to quantify the difference in the force induced against the fast and slow ramp load between the arm abductions under teeth non-clenching and clenching conditions. When the load of adduction moment was linearly increased, the abductor force increased to a maximal isometric contraction force (MICF) and further increased to a maximal eccentric contraction force (MECF) with forced adduction. The MICF measured under teeth clenching was significantly lower than that under non-clenching, despite no significant difference in the MECF between the two conditions. The reduction in MICF caused by teeth clenching was enhanced by increasing the velocity of the load. These results suggest that clenching inhibits abduction force only during isometric contraction phase. The invariability of MECF would indicate the lack of involvement of fatigue in such inhibitory effects of clenching. To discover the source of the inhibition, we have examined the effects of teeth clenching on the stretch reflex in the deltoid muscle. The stretch reflex of deltoid muscles was inhibited during clenching, contrary to what was expected from the Jendrassik maneuver. Taken together, our results suggest that the teeth clenching reduced the MICF by depressing the recruitment of deltoid motoneurones presumably via the presynaptic inhibition of spindle afferent inputs onto those motoneurones.

DOI： 10.1007/s00221-014-3919-8

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PubMed

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Federation of European Neuroscience Societies  

We previously showed that a positive covariability between intracortical excitatory synaptic actions onto the two layer three pyramidal cells (PCs) located in mutually adjacent columns is changed into a negative covariability by column-wise presynaptic inhibition of intracortical inputs, implicated as a basis for the desynchronization of inter-columnar synaptic actions. Here we investigated how the inter-columnar desynchronization is modulated by the strength of presynaptic inhibition or other factors, by using a mathematical model. Based on our previous findings on the paired-pulse depression (PPD) of intracortical excitatory postsynaptic currents (EPSCs) evoked in PCs located in the stimulated home column (HC) but no PPD in PCs located in the adjacent column (AC), a mathematical model of synaptic connections between PCs and inhibitory interneurons was constructed. When the paired-pulse ratio (PPR) was decreased beyond 0.80, the correlation coefficient between the two second EPSC amplitudes in the paired PCs located in the HC and AC and that in the paired PCs located in the same HC exhibited opposite changes, and reached a global negative maximum and local positive maximum, respectively, at almost the same PPR (0.40). At this PPR, the desynchronization between the two cell assemblies in mutually adjacent columns would be maximized. These positive and negative covariabilities were not produced without background oscillatory synchronization across columns and were enhanced by increasing the synchronization magnitude, indicating that the synchronization leads to the desynchronization. We propose that a slow oscillatory synchronization across columns may emerge following the liberation from the column-wise presynaptic inhibition of inter-columnar synaptic inputs.

DOI： 10.1111/ejn.12299

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Federation of European Neuroscience Societies  

Intracortical axons originating from pyramidal cells in layer 3 of the rat somatosensory cortex are shared between adjacent columns, and receive the presynaptic inhibition that is mediated by the GABA_B receptor. Synaptic actions by intracortical axons of single layer 3 pyramidal cells covary between the two adjacent columns in response to stimulation of layer 3 of either column. We examined whether GABA_B receptor-mediated presynaptic inhibition affects the covariability of synaptic actions by intracortical axons between adjacent columns in slice preparations of the rat barrel cortex. Paired stimulations of superficial layer 3 evoked first and second excitatory postsynaptic currents (EPSCs) of varying amplitudes, yielding varying paired-pulse depression of EPSCs in layer 3 pyramidal cells that were located in the stimulated column, but not in its adjacent column. The amplitude of the second EPSC was inversely proportional to that of the first EPSC in layer 3 pyramidal cells in the stimulated column, yielding a negative correlation coefficient between the first and second EPSCs. Baclofen and CGP55845 attenuated paired-pulse depression and abolished the inverse relationship. Simultaneous recordings from two layer 3 pyramidal cells in the stimulated and adjacent columns revealed a positive correlation between the paired first EPSC amplitudes and a negative correlation between the paired second EPSC amplitudes, which, respectively, indicate the positive and negative covariability of synaptic actions by intracortical axons between the two adjacent columns. These results suggest that GABA_B receptor-mediated presynaptic inhibition can reverse the positive covariability of inter-columnar synaptic actions, which may serve as a basis for inter-columnar desynchronisation.

DOI： 10.1111/ejn.12041

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Society  

Spindle Ia afferents may be differentially involved in voluntary isometric contraction, depending on the pattern of synaptic connections in spindle reflex pathways. We investigated how isometric contraction of masseter muscles is regulated through the activity of their muscle spindles that contain the largest number of intrafusal fibers among skeletal muscle spindles by examining the effects of vibration of muscle spindles on the voluntary isometric contraction. Subjects were instructed to hold the jaw at resting position by counteracting ramp loads applied on lower molar teeth. In response to the increasing-ramp load, the root mean square (RMS) of masseter EMG activity almost linearly increased under no vibration, while displaying a steep linear increase followed by a slower increase under vibration. The regression line of the relationship between the load and RMS was significantly steeper under vibration than under no vibration, suggesting that the subjects overestimated the ramp load and excessively counteracted it as reflected in the emergence of bite pressure. In response to the decreasing-ramp load applied following the increasing one, the RMS hardly decreased under vibration unlike under no vibration, leading to a generation of bite pressure even after the offset of the negative-ramp load until the vibration was ceased. Thus the subjects overestimated the increasing rate of the load while underestimating the decreasing rate of the load, due to the vibration-induced illusion of jaw opening. These observations suggest that spindle Ia/II inputs play crucial roles both in estimating the load and in controlling the isometric contraction of masseter muscles in the jaw-closed position.

DOI： 10.1152/jn.00997.2011

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PubMed

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Society for Neuroscience  

In the insular cortex, the primary gustatory area caudally adjoins the primary autonomic area that is involved in visceral sensory-motor integration. However, it has not been addressed whether neural activity in the gustatory insula (Gu-I) is coordinated with that in the autonomic insula (Au-I). We have demonstrated that TRPV1 activation in Gu-I induces theta-band synchronization between Gu-I and Au-I in rat slice preparations. Electron-microscopic immunohistochemistry revealed that TRPV1 immunoreactivity was much higher in Gu-I than in Au-I, and was mostly detected in dendritic spines receiving asymmetrical synapses. Whole-cell voltage-clamp recordings revealed that, in Gu-I, capsaicin-induced currents in layer 3 (L3) pyramidal cells (PCs) displayed no apparent desensitization, while those in layer 5 (L5) PCs displayed Ca²⁺-dependent desensitization, suggesting that L3 and L5 PCs respond differentially to TRPV1 activation. Voltage-sensitive dye imaging demonstrated that TRPV1 activation in Gu-I can alter an optical response with a monophasic and columnar temporospatial pattern evoked within Gu-I into an oscillatory one extending over Gu-I and Au-I. Power and cross-power spectral analyses of optical responses revealed theta-band synchronization between Gu-I and Au-I. Whole-cell current-clamp recordings demonstrated that such theta-band waves were mediated by sustained rhythmic firings at 4 and 8 Hz in L3 and L5 PCs, respectively. These results strongly suggested that theta-band oscillatory neural coordination between Gu-I and Au-I was induced by two distinct TRPV1-mediated theta-rhythm firings in L3 and L5 PCs in Gu-I. This network coordination induced by TRPV1 activation could be responsible for autonomic responses to tasting and ingesting spicy foods.

DOI： 10.1523/JNEUROSCI.5906-11.2012

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Society for Neuroscience  

Leak K⁺ conductance generated by TASK1/3 channels is crucial for neuronal excitability. However, endogenous modulators activating TASK channels in neurons remained unknown. We previously reported that in the presumed cholinergic neurons of the basal forebrain (BF), activation of NO-cGMP-PKG (protein kinase G) pathway enhanced the TASK1-like leak K⁺ current (I_K-leak). As 8-Br-cGMP enhanced the I_K-leak mainly at pH 7.3 as if changing the I_K-leak from TASK1-like to TASK3-like current, such an enhancement of the I_K-leak would result either from an enhancement of hidden TASK3 component or from an acidic shift in the pH sensitivity profile of TASK1 component. In view of the report that protonation of TASK channel decreases its open probability, the present study was designed to examine whether the activation of PKG increases the conductance of TASK1 channels by reducing their binding affinity for H⁺, i.e., by increasing K_d for protonation, or not. We here demonstrate that PKG activation and inhibition respectively upregulate and downregulate TASK1 channels heterologously expressed in PKG-loaded HEK293 cells at physiological pH, by causing shifts in the K_d in the acidic and basic directions, respectively. Such PKG modulations of TASK1 channels were largely abolished by mutating pH sensor H98. In the BF neurons that were identified to express ChAT and TASK1 channels, similar dynamic modulations of TASK1-like pH sensitivity of I_K-leak were caused by PKG. It is strongly suggested that PKG activation and inhibition dynamically modulate TASK1 currents at physiological pH by bidirectionally changing K_d values for protonation of the extracellular pH sensors of TASK1 channels in cholinergic BF neurons.

DOI： 10.1523/JNEUROSCI.5407-09.2010

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PubMed

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Wiley Interscience  

Rundown is ubiquitously seen in response to repetitive activation of receptor or ion channels as a use-dependent down-regulation through various mechanisms. In contrast to AMPA receptors, gamma-aminobutyric acid type A receptor (GABA_AR) are believed to display no rapid use-dependent down-regulation. We report here a rapid use-dependent down-regulation of GABA_AR in primary sensory neurons of rat mesencephalic trigeminal nucleus (MTN), which express synaptic GABA_ARs in addition to extrasynaptic ones, unlike other primary sensory neurons. When muscimol was repetitively puff-applied to an MTN neuron every 2 min before, during, and after the muscimol bath application for 5 min, both the GABA_A responses obtained under both current- and voltage-clamp conditions were almost completely depressed during the bath application. However, the former and latter GABA_A responses recovered to 26% +/- 7% and 36% +/- 7% of their control amplitudes, respectively, 15 min after washout of the bath-applied muscimol. By contrast, when examined in the presence of chelerythrine, a protein kinase C (PKC) inhibitor, together with a strin gent chelation of intracellular Ca²⁺, the puff responses were almost completely recovered, whereas those were recovered to 40-60% of the control by either chelerythrine or EGTA alone. A phosphatidylinositol 3-kinase inhibitor (PI3K), wortmannin, which blocks various signal transductions, including vesicular trafficking, significantly enhanced the rundown of the puff responses examined every 2 min. These findings indicate that the rundown of GABA_A response in MTN neurons is mediated by the use-dependent down-regulation of GABA_AR, which is reversed by PKC inhibition together with intracellular Ca²⁺ chelation, while being facilitated by PI3K inhibition.

DOI： 10.1002/jnr.22141

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Society  

In an earlier study, we demonstrated that nitric oxide (NO) causes the long-lasting membrane hyperpolarization in the presumed basal forebrain cholinergic (BFC) neurons by cGMP-PKG-dependent activation of leak K⁺ currents in slice preparations. In the present study, we investigated the ionic mechanisms underlying the long-lasting membrane hyperpolarization with special interest in the pH sensitivity because 8-Br-cGMP-induced K⁺ current displayed Goldman-Hodgkin-Katz rectification characteristic of TWIK-related acid-sensitive K⁺ (TASK) channels. When examined with the ramp command pulse depolarizing from -130 to -40 mV, the presumed BFC neurons displayed a pH-sensitive leak K⁺ current that was larger in response to pH decrease from 8.3 to 7.3 than in response to pH decrease from 7.3 to 6.3. This K⁺ current was similar to TASK1 current in its pH sensitivity, whereas it was highly sensitive to Ba2+, unlike TASK1 current. The 8-Br-cGMP-induced K⁺ currents in the presumed BFC neurons were almost completely inhibited by lowering external pH to 6.3 as well as by bath application of 100 microM Ba2+ , consistent with the nature of the leak K⁺ current expressed in the presumed BFC neurons. After 8-Br-cGMP application, the K⁺ current obtained by pH decrease from 7.3 to 6.3 was larger than that obtained by pH decrease from pH 8.3 to 7.3, contrary to the case seen in the control condition. These observations strongly suggest that 8-Br-cGMP activates a pH- and Ba2+ -sensitive leak K⁺ current expressed in the presumed BFC neurons by modulating its pH sensitivity.

DOI： 10.1152/jn.01051.2007

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Society for Neuroscience  

The columnar organization is most apparent in the whisker barrel cortex but seems less apparent in the gustatory insular cortex. We addressed here whether there are any differences between the two cortices in columnar information processing by comparing the spatiotemporal patterns of excitation spread in the two cortices using voltage-sensitive dye imaging. In contrast to the well known excitation spread in the horizontal direction in layer II/III induced in the barrel cortex by layer IV stimulation, the excitation caused in the insular cortex by stimulation of layer IV spread bidirectionally in the vertical direction into layers II/III and V/VI, displaying a columnar image pattern. Bicuculline or picrotoxin markedly extended the horizontal excitation spread in layer II/III in the barrel cortex, leading to a generation of excitation in the underlying layer V/VI, whereas those markedly increased the amplitude of optical responses throughout the whole column in the insular cortex, subsequently widening the columnar image pattern. Such synchronous activities as revealed by the horizontal and vertical excitation spreads were consistently induced in the barrel and insular cortices, respectively, even by stimulation of different layers with varying intensities. Thus, a unique functional column existed in the insular cortex, in which intracolumnar communication between the superficial and deep layers was prominent, and GABA_A action is involved in the inhibition of the intracolumnar communication in contrast to its involvement in intercolumnar lateral inhibition in the barrel cortex. These results suggest that the columnar information processing may not be universal across the different cortical areas.

DOI： 10.1523/JNEUROSCI.0172-08.2008

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Society  

Learning and memory are critically dependent on basal forebrain cholinergic (BFC) neuron excitability, which is modulated profoundly by leak K⁺ channels. Many neuro-modulators closing leak K⁺ channels have been reported, whereas their endogenous opener remained unknown. We here demonstrate that nitric oxide (NO) can be the endogenous opener of leak K⁺ channels in the presumed BFC neurons. Bath application of 1 mM S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, induced a long-lasting hyperpolarization, which was often interrupted by a transient depolarization. Soluble guanylyl cyclase inhibitors prevented SNAP from inducing hyperpolarization but allowed SNAP to cause depolarization, whereas bath application of 0.2 mM 8-bromo-guanosine-3',5' -cyclomonophosphate (8-Br-cGMP) induced a similar long-lasting hyperpolarization alone. These observations indicate that the SNAP-induced hyperpolarization and depolarization are mediated by the cGMP-dependent and -independent processes, respectively. When examined with the ramp command pulse applied at -70 mV under the voltage-clamp condition, 8-Br-cGMP application induced the outward current that reversed at K⁺ equilibrium potential (E-K) and displayed Goldman-Hodgkin-Katz rectification, indicating the involvement of voltage-independent K⁺ current. By contrast, SNAP application in the presumed BFC neurons either dialyzed with the GTP-free internal solution or in the presence of 10 microM Rp-8-bromo-beta-phenyl-1, N-2-ethenoguanosine 3',5' -cyclic monophosphorothioate sodium salt, a protein kinase G (PKG) inhibitor, induced the inward current that reversed at potentials much more negative than E K and close to the reversal potential of Na⁺ -K⁺ pump current. These observations strongly suggest that NO activates leak K⁺ channels through cGMP-PKG-dependent pathway to markedly decrease the excitability in BFC neurons, while NO simultaneously causes depolarization by the inhibition of Na⁺ -K⁺ pump through ATP depletion.

DOI： 10.1152/jn.00536.2007

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Society  

It was recently shown that the persistent Na⁺ current (I_NaP) is generated in the proximal axon in response to somatic depolarization in neocortical pyramidal neurons, although the involvement of I_NaP in spike initiation is still unclear. Here we show a potential role of I_NaP in spike initiation of primary sensory neurons in the mesencephalic trigeminal nucleus (MTN) that display a back-propagation of the spike initiated in the stem axon toward the soma in response to soma depolarization. Riluzole (10 microM) and tetrodotoxin (TTX, 10 nM) caused an activation delay or a stepwise increase in the threshold for evoking soma spikes (S-spikes) without affecting the spike itself. Simultaneous patch-clamp recordings from the soma and axon hillock (AH) revealed that bath application of 50 nM TTX increased the delay in spike activation in response to soma depolarization, leaving the spike-backpropagation time from the AH to soma unchanged. This indicates that the increase in activation delay occurred in the stem axon. Furthermore, under a decreasing intracellular concentration gradient of QX-314 from the soma to AH created by QX-314-containing and QX-314-free patch pipettes, the amplitude and maximum rate of rise (MRR) of AH-spikes decreased with an increase in the activation delay following repetition of current-pulse injections, whereas S-spikes displayed decreases of considerably lesser degree in amplitude and MRR. This suggests that compared to S-spikes, AH-spikes more accurately reflect the attenuation of axonal spike by QX-314, consistent with the nature of spike backpropagation. These observations strongly suggest that low-voltage -activated I_NaP is involved in spike initiation in the stem axon of MTN neurons.

DOI： 10.1152/jn.01191.2006

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PubMed

Language：English   Publishing type：Doctoral thesis  

The axon initial segment plays important roles in spike initiation and invasion of axonal spikes into the soma. Among primary sensory neurons, those in the mesencephalic trigeminal nucleus (MTN) are exceptional in their ability to initiate soma spikes (S-spikes) in response to synaptic inputs, consequently displaying two kinds of S-spikes, one caused by invasion of an axonal spike arising from the sensory receptor and the other initiated by somatic inputs. We investigated where spikes are initiated in such MTN neurons and whether there are any differences between the two kinds of S-spikes. Simultaneous patch-clamp recordings from the soma and axon hillock revealed a spike-backpropagation from the spike-initiation site in the stem axon to the soma in response to 1-ms somatic current pulse, which disclosed the delayed emergence of S-spikes after the current-pulse offset. These initiated S-spikes were smaller in amplitude than S-spikes generated by stimulation of the stem axon; however, 4-AP (<= 0.5 mM) eliminated the amplitude difference. Furthermore, 4-AP dramatically shortened the delay in spike initiation without affecting the spike-backpropagation time in the stem axon, whereas it substantially prolonged the refractory period of S-spikes arising from axonal-spike invasion without significantly affecting that of presumed axonal spikes. These observations suggest that 4-AP sensitive K⁺ currents exert two opposing effects on S-spikes depending on their origins: suppression of spike initiation and facilitation of axonal-spike invasion at higher frequencies. Consistent with these findings, strong immunoreactivities for Kv1.1 and Kv1.6, among 4-AP-sensitive and low-voltage-activated Kv1 family examined, were detected in the soma but not in the stem axon of MTN neurons.

DOI： 10.1152/jn.00176.2006

PubMed

Other Link： http://jn.physiology.org/content/96/4/1887.long

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Society  

The axon initial segment plays important roles in spike initiation and invasion of axonal spikes into the soma. Among primary sensory neurons, those in the mesencephalic trigeminal nucleus (MTN) are exceptional in their ability to initiate soma spikes (S-spikes) in response to synaptic inputs, consequently displaying two kinds of S-spikes, one caused by invasion of an axonal spike arising from the sensory receptor and the other initiated by somatic inputs. We investigated where spikes are initiated in such MTN neurons and whether there are any differences between the two kinds of S-spikes. Simultaneous patch-clamp recordings from the soma and axon hillock revealed a spike-backpropagation from the spike-initiation site in the stem axon to the soma in response to 1-ms somatic current pulse, which disclosed the delayed emergence of S-spikes after the current-pulse offset. These initiated S-spikes were smaller in amplitude than S-spikes generated by stimulation of the stem axon; however, 4-AP (<= 0.5 mM) eliminated the amplitude difference. Furthermore, 4-AP dramatically shortened the delay in spike initiation without affecting the spike-backpropagation time in the stem axon, whereas it substantially prolonged the refractory period of S-spikes arising from axonal-spike invasion without significantly affecting that of presumed axonal spikes. These observations suggest that 4-AP sensitive K⁺ currents exert two opposing effects on S-spikes depending on their origins: suppression of spike initiation and facilitation of axonal-spike invasion at higher frequencies. Consistent with these findings, strong immunoreactivities for Kv1.1 and Kv1.6, among 4-AP-sensitive and low-voltage-activated Kv1 family examined, were detected in the soma but not in the stem axon of MTN neurons.

DOI： 10.1152/jn.00176.2006

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：International Brain Research Organization  

In neurons of dorsal motor nucleus of the vagus that is involved in the gastric motility and possibly emesis, application of 5-hydroxytryptamine produces membrane depolarization, and suppresses spike-repolarization and spikeafterhyperpolarization, suggesting divergent effects of 5-hydroxytryptamine through activating multiple subtypes of 5-hydroxytryptamine receptors. However, only the role of 5-hydroxytryptamine 2A receptors has been established to be responsible for the depolarization, and the mechanisms underlying the modulation of spikes remain unknown although a role of 5-hydroxytryptamine 4 receptors was implicated in modulations of spikes. There is now increasing evidence for the role of 5-hydroxytryptamine receptors in neurons involved in generating emesis following administration of anticancer drug. Since antagonists of 5-hydroxytryptamine 3/4 receptors are widely used as anti-emetic drugs, we have reevaluated the functional roles of 5-hydroxytryptamine 3/4 receptors of dorsal motor nucleus of the vagus neurons, especially in modulating transient outward currents that are presumed to be involved in spike-repolarization and spikeafterhyperpolarization. Whole-cell patch-clamp recordings were made from the dorsal motor nucleus of the vagus neurons, which were identified by a retrograde tracing method with dextran-tetramethyrhodamine-lysine injected into a bundle of abdominal vagus nerves. Under a voltage-clamp condition, dorsal motor nucleus of the vagus neurons expressed a prominent A-like current. The activation of 5-hydroxytryptamine 3 receptors reversibly increased the resting membrane conductance while the activation of 5-hydroxytryptamine 4 receptors led to an almost irreversible decrease in the A-like current. A long-lasting suppression of A-like current by transient activation of 5-hydroxytryptamine 4 receptors would result in a long-lasting increase in the excitability of dorsal motor nucleus of the vagus neurons, which might be involved in generation of the long-lasting facilitation of gastric motility or in generation of the long-lasting gastric relaxation through the activation of enteric non-adrenergic non-cholinergic neurons as implicated in the delayed emesis induced by anticancer drugs.

DOI： 10.1016/j.neuroscience.2006.04.025

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Society for Neuroscience  

The Na⁺ -K⁺ pump current (I_p) and the h-current (I_h) flowing through hyperpolarization-activated channels (h-channels) participate in generating the resting potential. These two currents are thought to be produced independently. We show here bidirectional interactions between Na⁺-K⁺ pumps and h-channels in mesencephalic trigeminal neurons. Activation of I_h leads to the generation of two types of ouabain-sensitive I_p with temporal profiles similar to those of instantaneous and slow components of I_h, presumably reflecting Na⁺ transients in a restricted cellular space. Moreover, the Ip activated by instantaneous I_h can facilitate the subsequent activation of slow I_h. Such counteractive and cooperative interactions were also disclosed by replacing extracellular Na⁺ with Li⁺, which is permeant through h-channels but does not stimulate the Na⁺ -K⁺ pump as strongly as Na⁺ ions. These observations indicate that the interactions are bidirectional and mediated by Na⁺ ions. Also after substitution of extracellular Na⁺ with Li⁺, the tail I_h was reduced markedly despite an enhancement of I_h itself, attributable to a negative shift of the reversal potential for I_h presumably caused by intracellular accumulation of Li⁺ ions. This suggests the presence of a microdomain where the interactions can take place. Thus, the bidirectional interactions between Na⁺ -K⁺ pumps and h-channels are likely to be mediated by Na⁺ microdomain. Consistent with these findings, hyperpolarization-activated and cyclic nucleotide-modulated subunits (HCN1/2) and the Na⁺ -K⁺ pump alpha3 isoform were colocalized in plasma membrane of mesencephalic trigeminal neurons having numerous spines.

DOI： 10.1523/JNEUROSCI.5641-03.2004

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：International Brain Research Organization  

Intracellular recordings were obtained from rat presumed jaw-closing motoneurons in slice preparations to investigate the involvement of the serotonin, (5-HT₇) receptors in serotonergic inhibition of the postspike medium-duration afterhyperpolarization (mAHP) and enhancement of the afterdepolarization (ADP). 5-HT-induced suppression of the mAHP and enhancement of the ADP were mimicked by application of the 5-HT_1A/7 receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and antagonized by the 5-HT_2/6/7 receptor antagonist clozapine, whereas the 5-HT₂ receptor agonist alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT) did not affect the mAHP and ADP 8-OH-DPAT-induced attenuation of the mAHP and enhancement of the ADP were also antagonized by clozapine and another 5-HT_2/6/7 receptor antagonist ritanserin, whereas the 5-HT_1A receptor antagonist pindolol failed to block the 8-OH-DPAT-induced effects on the mAHP and ADP 8-OH-DPAT-induced suppression of the mAHP and enhancement of the ADP were also antagonized by a protein kinase A (PKA) inhibitor H89, whereas 8-OH-DPAT could inhibit the mAHP and enhance the ADP in the presence of a protein kinase C (PKC) inhibitor chelerythrine. The 8-OH-DPAT-induced suppression of the mAHP was enhanced under raised [Ca²⁺]_o and this enhancement was reduced by chelerythrine. It is suggested that the 5-HT₇ receptors are involved in 5-HT-induced attenuation of the mAHP and enhancement of the ADP through activation of PKA, and the attenuation of mAHP through the 5-HT₇ receptors is enhanced under raised [Ca²⁺]_o by PKC activation.

DOI： 10.1016/S0006-8993(02)03286-9

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PubMed

Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Dental Association, International Association for Dental Research, American Association for Dental Research  

It has been difficult for investigators to simultaneously and reliably evaluate bite force in the intercuspal position with the area and location of occlusal contacts. This study was designed to investigate the variations in these parameters with respect to two factors: three levels of clenching and the preferred chewing side. Human subjects with normal occlusion were examined with a recently developed system (Dental Prescale Occluzer, Fuji Film,Tokyo, Japan). The three levels of clenching intensity were assessed by masseteric EMG activity and included the maximum voluntary contraction, and 30% and 60% of the maximum. The results indicated that the bite force and occlusal contact area on the whole dental arch increased with clenching intensity. In contrast, the average bite pressure, obtained by dividing the bite force by the contact area, remained unchanged regardless of the clenching intensity. As the clenching intensity increased, the medio-lateral position of the bite force balancing point shifted significantly(P < 0.01) from the preferred chewing side toward the midline. The antero-posterior position remained stable in a range between the distal third of the first molar and the mesial third of the second molar. The bite force and occlusal contact area, which were mainly on the molars, increased with the clenching intensity, whereas the proportions of these two variables on each upper tooth usually did not change significantly. The exception was the second molar on the non-preferred chewing side. When comparisons were made between pairs of specific upper teeth of same name, usually no significant difference was found in bite force or occlusal contact area, regardless of the clenching level. Again, the exception to this observation was the second molar on the preferred chewing side, which had a larger area at the 30% clenching level. The results in normal subjects suggest that as the clenching intensity increases in the intercuspal position, the bite force adjusts to a position where it is well-balanced. This adjustment may prevent damage and overload to the teeth and temporomandibular joints.

DOI： 10.1177/00220345990780070801

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PubMed

Language：English   Publishing type：Article, review, commentary, editorial, etc. (international conference proceedings)   Publisher：Springer Japan  

The slow-closing phase of the mastication cycle plays a major role in the mastication of foods. However, the neuronal mechanism underlying the slow-closing phase remains unknown. During the slow-closing phase, isometric contraction of jaw-closing muscles is developed through the recruitment of jaw-closing motoneurons (MNs). It is well established that motor units are recruited depending on the order of sizes or input resistances (IRs) of MNs, which is known as the size principle. TASK 1/3 channels are recently found to be the molecular correlates of the IR, and also found to be expressed in the masseter MNs. The orderly recruitment of masseter MNs may be modified by the activity of TASK1/3 channels. In this chapter, we discuss the synaptic mechanisms underlying the orderly recruitment of masseter MNs that occurs during the slow-closing phase, together with the mechanism for the modulation of the orderly recruitment of motor units.

DOI： 10.1007/978-4-431-99644-6_9

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)   Publisher：Elsevier  

The slow-closing phase of the mastication cycle plays a major role in the mastication of foods. However, the neuronal mechanism underlying the slow-closing phase remains unknown. The isometric contraction of jaw-closing muscles is developed through the recruitment of jaw-closing motoneurons during the slow-closing phase. It is well established that motor units are recruited depending on the order of sizes or input resistances (IRs) of motoneurons, which is known as the size principle. Two-pore-domain acid-sensitive K⁺ (TASK1/3) channels are recently found to be the molecular correlates of the IR, and also found to be expressed in the masseter motoneurons. Here, we addressed the question whether spindle Ia inputs onto masseter motoneurons can induce the orderly recruitment of motoneurons in slice preparations of the rat brain using voltage-sensitive dye imaging and whole-cell patch-clamp methods. Voltage-sensitive dye imaging revealed the recruitment of many motoneurons in the whole nucleus of masseter in response to repetitive stimulation of the presumed spindle Ia inputs. Dual whole-cell recordings obtained from two adjacent motoneurons revealed the IR-ordered recruitment of motoneurons in response to repetitive stimulation of the presumed spindle Ia inputs. Thus, Ia inputs are likely to play a crucial role in the orderly recruitment of motoneurons of the trigeminal motor nucleus, which would be progressed during the slow-closing phase of the mastication cycle. Possible involvements of TASK channels in the orderly recruitment are discussed.

DOI： 10.1016/B978-0-444-53613-6.00011-3

PubMed

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)   Publisher：Japanese Association for Oral Biology  

DOI： 10.1016/S1349-0079(10)80013-1

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)   Publisher：Japanese Association for Dental Science  

DOI： 10.1016/j.jdsr.2009.12.002

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (other)   Publisher：大阪大学出版会  

Other Link： http://www.osaka-up.or.jp/books/ISBN978-4-87259-233-7.html

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)   Publisher：The Korean Academy of Oral Biology  

In the primary sensory neuron of the mesencephalic trigeminal nucleus (MTN), the peripheral axon supplies a large number of annulospiral endings surrounding intrafusal fibers encapsulated in single muscle spindles while the central axon sends only a few number of synapses onto single alpha-motoneuron.(alpha-MN). Therefore, the alpha-gamma linkage is thought to be very crucial in the jaw-closing movement. Spike activity in a gamma-motoneuron (gamma-MN) would induce a large number of impulses in single peripheral axons by activating many intrafusal fibers simultaneously, subsequently causing an activation of alpha-MN in spite of the small number of synapses. Thus, the activity of gamma-MN may be vital for modulation of jaw-closing movements. Independently of such a spindle activity modulated by gamma-MN, somatic depolarization in MTN neurons is known to trigger the oscillatory spike activity. Nevertheless, the trafficking of these spikes arising from the two distinct sources of MTN neurons is not well understood. In this short review, switching among multiple functional modes of MTN neurons is discussed. Subsequently, it will be discussed which mode can support the alpha-gamma linkage. In our most recent study, simultaneous patch-clamp recordings from the soma and axon hillock revealed a spike-back-propagation from the spike-initiation site in the stem axon to the soma in response to a somatic current pulse. The persistent Na⁺ current was found to be responsible for the spike-initiation in the stem axon, the activation threshold of which was lower than those of soma spikes. Somatic inputs or impulses arising from the sensory ending, whichever trigger spikes in the stem axon first, would be forwarded through the central axon to the target synapse. We also demonstrated that at hyperpolarized membrane potentials, 4-AP-sensitive K⁺ current (I_K4AP) exerts two opposing effects on spikes depending on their origins; the suppression of spike initiation by increasing the apparent electrotonic distance between the soma and the spike-initiation site, and the facilitation of axonal spike invasion at higher frequencies by decreasing the spike duration and the refractory period. Through this mechanism, the spindle activity caused by gamma-MN would be safely forwarded to alpha-MN. Thus, soma spikes shaped differentially by this I_K4AP depending on their origins would reflect which one of the two inputs was forwarded to the target synapses.

Other Link： http://www.kijob.or.kr/journal/article.php?code=1069

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (other)   Publisher：大阪大学出版会  

Other Link： http://www.osaka-up.or.jp/books/ISBN978-4-87259-185-9.html

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)   Publisher：医歯薬出版  

Other Link： https://www.ishiyaku.co.jp/search/details.aspx?bookcode=021022

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)   Publisher：Japanese Association for Dental Science  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (bulletin of university, research institution)   Publisher：昭和歯学会  

咀嚼する食品の物理的性状にしたがって咀嚼筋活動は適切に調節されるが、この調節には歯根膜感覚受容器と閉口筋筋紡錘からの感覚情報が重要な役割を果たしている。三叉神経運動核周囲の網様体には、口腔領域からの感覚情報が入力し、出力を三叉神経運動核に送るニューロンが存在する。このようなニューロンは咀嚼筋活動の調節に関与している可能性がある。閉口筋運動ニューロンに口腔領域からの感覚によって修飾を受けた咀嚼の運動指令が入力するが、同時にセロトニン入力によって興奮性が増大する等の変調を受ける。以上のようなメカニズムは、咀嚼する食物の性状に見合った適切な咀嚼力の発現に役立っていると考えられる。

CiNii Research

Other Link： https://www.jstage.jst.go.jp/article/dentalmedres1981/21/1/21_58/_article/-char/ja/

Event date： 2015.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Toki Messe Niigata Convention Center (Niigata, Japan)  

CiNii Research

Event date： 2015.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Toki Messe Niigata Convention Center (Niigata, Japan)  

CiNii Research

Event date： 2015.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Toki Messe Niigata Convention Center (Niigata, Japan)  

CiNii Research

Event date： 2015.5

Language：English   Presentation type：Poster presentation  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Symposium, workshop panel (nominated)  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Symposium, workshop panel (nominated)  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Symposium, workshop panel (nominated)  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Poster presentation  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Poster presentation  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Poster presentation  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Poster presentation  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2015.5

Language：English   Presentation type：Poster presentation  

Venue：Osaka University Nakanoshima Center (Osaka, Japan)  

Event date： 2014.11

Language：English   Presentation type：Poster presentation  

Venue：Walter E. Washington Convention Center (Washington, DC, USA)  

Event date： 2014.11

Language：English   Presentation type：Poster presentation  

Venue：Walter E. Washington Convention Center (Washington, DC, USA)  

Event date： 2014.11

Language：English   Presentation type：Poster presentation  

Venue：Walter E. Washington Convention Center (Washington, DC, USA)  

Event date： 2014.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Fukuoka International Congress Center (Fukuoka, Japan)  

CiNii Research

Event date： 2014.9

Language：English   Presentation type：Poster presentation  

Venue：Pacifico Yokohama Conference Center (Yokohama, Japan)  

Event date： 2014.9

Language：English   Presentation type：Poster presentation  

Venue：Pacifico Yokohama Conference Center (Yokohama, Japan)  

Event date： 2014.9

Language：English   Presentation type：Poster presentation  

Venue：Pacifico Yokohama Conference Center (Yokohama, Japan)  

Event date： 2014.9

Language：English   Presentation type：Poster presentation  

Venue：Pacifico Yokohama Conference Center (Yokohama, Japan)  

Event date： 2013.11

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2013.11

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2013.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Okayama Convention Center (Okayama, Japan)  

CiNii Research

Event date： 2013.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Okayama Convention Center (Okayama, Japan)  

CiNii Research

Event date： 2013.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Okayama Convention Center (Okayama, Japan)  

CiNii Research

Event date： 2013.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Okayama Convention Center (Okayama, Japan)  

CiNii Research

Event date： 2013.9

Language：Japanese   Presentation type：Poster presentation  

Venue：Okayama Convention Center (Okayama, Japan)  

CiNii Research

Event date： 2013.9

Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

Venue：仙台市民会館 (仙台市)  

Event date： 2013.9

Language：English   Presentation type：Symposium, workshop panel (nominated)  

Venue：浜松医科大学 (浜松市)  

Event date： 2013.6

Language：English   Presentation type：Poster presentation  

Venue：Kyoto International Conference Center (Kyoto, Japan)  

Event date： 2013.3

Language：English   Presentation type：Poster presentation  

Venue：タワーホール船堀 (東京都江戸川区)  

Event date： 2012.10

Language：English   Presentation type：Poster presentation  

Venue：Ernest N. Morial Convention Center (New Orleans, LA, USA)  

Event date： 2012.10

Language：English   Presentation type：Poster presentation  

Venue：Ernest N. Morial Convention Center (New Orleans, LA, USA)  

Event date： 2012.9

Language：English   Presentation type：Poster presentation  

Venue：Nagoya Congress Center (Nagoya, Japan)  

Event date： 2011.11

Language：English   Presentation type：Poster presentation  

Venue：Walter E. Washington Convention Center (Washington, DC, USA)  

Event date： 2011.9 - 2011.10

Language：Japanese   Presentation type：Poster presentation  

Venue：長良川国際会議場 (岐阜市)  

CiNii Research

Event date： 2011.9 - 2011.10

Language：Japanese   Presentation type：Poster presentation  

Venue：長良川国際会議場 (岐阜市)  

CiNii Research

Event date： 2011.9 - 2011.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：長良川国際会議場 (岐阜市)  

CiNii Research

Event date： 2011.9 - 2011.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：長良川国際会議場 (岐阜市)  

CiNii Research

Event date： 2011.9 - 2011.10

Language：Japanese   Presentation type：Poster presentation  

Venue：長良川国際会議場 (岐阜市)  

CiNii Research

Event date： 2011.3

Language：English   Presentation type：Poster presentation  

Venue：パシフィコ横浜 (横浜市)  

Event date： 2011.3

Language：English   Presentation type：Poster presentation  

Venue：パシフィコ横浜 (横浜市)  

Event date： 2011.3

Language：English   Presentation type：Poster presentation  

Venue：パシフィコ横浜 (横浜市)  

Event date： 2010.11

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2010.11

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2010.11

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2010.11

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2010.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：大阪大学吹田キャンパス 銀杏会館 (吹田市)  

CiNii Research

Event date： 2010.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：大阪大学吹田キャンパス 銀杏会館 (吹田市)  

CiNii Research

Event date： 2009.10

Language：English   Presentation type：Poster presentation  

Venue：McCormick Place (Chicago, IL, USA)  

Event date： 2009.9

Language：English   Presentation type：Poster presentation  

Venue：名古屋国際会議場 (名古屋市)  

Event date： 2009.9

Language：English   Presentation type：Poster presentation  

Venue：名古屋国際会議場 (名古屋市)  

Event date： 2009.9

Language：Japanese   Presentation type：Poster presentation  

Venue：朱鷺メッセ 新潟コンベンションセンター (新潟市)  

CiNii Research

Event date： 2009.9

Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

Venue：朱鷺メッセ 新潟コンベンションセンター (新潟市)  

Event date： 2009.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：朱鷺メッセ 新潟コンベンションセンター (新潟市)  

CiNii Research

Event date： 2009.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：朱鷺メッセ 新潟コンベンションセンター (新潟市)  

CiNii Research

Event date： 2009.9

Language：Japanese   Presentation type：Poster presentation  

Venue：朱鷺メッセ 新潟コンベンションセンター (新潟市)  

CiNii Research

Event date： 2009.7 - 2009.8

Language：English   Presentation type：Poster presentation  

Venue：国立京都国際会館 (京都市)  

Event date： 2009.7 - 2009.8

Language：English   Presentation type：Poster presentation  

Venue：国立京都国際会館 (京都市)  

Event date： 2009.7 - 2009.8

Language：English   Presentation type：Poster presentation  

Venue：国立京都国際会館 (京都市)  

Event date： 2009.1

Language：English   Presentation type：Symposium, workshop panel (nominated)  

Venue：仙台国際センター (仙台市)  

Event date： 2008.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：国立循環器病センター研究所 (吹田市)  

CiNii Research

Event date： 2008.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：国立循環器病センター研究所 (吹田市)  

CiNii Research

Event date： 2008.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：国立循環器病センター研究所 (吹田市)  

CiNii Research

Event date： 2008.7

Language：English   Presentation type：Poster presentation  

Venue：Palexpo Conference Center (Geneva, Switzerland)  

Event date： 2008.7

Language：English   Presentation type：Poster presentation  

Venue：Palexpo Conference Center (Geneva, Switzerland)  

Event date： 2008.7

Language：English   Presentation type：Poster presentation  

Venue：Palexpo Conference Center (Geneva, Switzerland)  

Event date： 2007.11

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2007.9

Language：English   Presentation type：Poster presentation  

Venue：パシフィコ横浜 (横浜市)  

Event date： 2007.9

Language：English   Presentation type：Poster presentation  

Venue：パシフィコ横浜 (横浜市)  

Event date： 2007.9

Language：English   Presentation type：Poster presentation  

Venue：パシフィコ横浜 (横浜市)  

Event date： 2007.8

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：北海道大学・学術交流会館 (札幌市)  

CiNii Research

Event date： 2006.10

Language：English   Presentation type：Poster presentation  

Venue：Georgia World Congress Center (Atlanta, GA, USA)  

Event date： 2006.9

Language：Japanese   Presentation type：Poster presentation  

Venue：鶴見大学歯学部 (横浜市)  

CiNii Research

Event date： 2006.9

Language：Japanese   Presentation type：Poster presentation  

Venue：鶴見大学歯学部 (横浜市)  

CiNii Research

Event date： 2006.9

Language：Japanese   Presentation type：Poster presentation  

Venue：鶴見大学歯学部 (横浜市)  

CiNii Research

Event date： 2006.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：大阪歯科大学楠葉学舎 (枚方市)  

CiNii Research

Event date： 2005.11

Language：English   Presentation type：Poster presentation  

Venue：Walter E. Washington Convention Center (Washington, DC, USA)  

Event date： 2005.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：滋賀医科大学 (大津市)  

CiNii Research

Event date： 2004.11

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：京都大学医学部内 芝蘭会館 (京都市)  

CiNii Research

Event date： 2004.10

Language：English   Presentation type：Poster presentation  

Venue：San Diego Convention Center (San Diego, CA, USA)  

Event date： 2004.9

Language：Japanese   Presentation type：Poster presentation  

Venue：広島国際会議場・広島大学歯学部・広仁会館 (広島市)  

CiNii Research

Event date： 2004.9

Language：Japanese   Presentation type：Poster presentation  

Venue：広島国際会議場・広島大学歯学部・広仁会館 (広島市)  

CiNii Research

Event date： 2004.9

Language：Japanese   Presentation type：Poster presentation  

Venue：広島国際会議場・広島大学歯学部・広仁会館 (広島市)  

CiNii Research

Event date： 2003.11

Language：English   Presentation type：Poster presentation  

Venue：Ernest N. Morial Convention Center (New Orleans, LA, USA)  

Event date： 2003.9

Language：Japanese   Presentation type：Poster presentation  

Venue：ホテルメトロポリタン盛岡・盛岡市民文化ホール (盛岡市)  

CiNii Research

Event date： 2003.8

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：京都府立医科大学 (京都市)  

CiNii Research

Event date： 2002.11

Language：English   Presentation type：Poster presentation  

Venue：Orange County Convention Center (Orlando, IL, USA)  

Event date： 2002.11

Language：English   Presentation type：Poster presentation  

Venue：Orange County Convention Center (Orlando, IL, USA)  

Event date： 2002.11

Language：English   Presentation type：Poster presentation  

Venue：Orange County Convention Center (Orlando, IL, USA)  

Event date： 2002.10

Language：Japanese   Presentation type：Poster presentation  

Venue：学術総合センター・学士会館 (東京都千代田区)  

CiNii Research

Event date： 2002.10

Language：Japanese   Presentation type：Poster presentation  

Venue：学術総合センター・学士会館 (東京都千代田区)  

CiNii Research

Event date： 2001.9

Language：English   Presentation type：Poster presentation  

Venue：Kyoto International Conference Center (Kyoto, Japan)  

CiNii Research

Event date： 2001.9

Language：Japanese   Presentation type：Poster presentation  

Venue：大宮ソニックシティ (さいたま市)  

CiNii Research

Event date： 2001.9

Language：Japanese   Presentation type：Poster presentation  

Venue：大宮ソニックシティ (さいたま市)  

CiNii Research

Event date： 2000.9 - 2000.10

Language：Japanese   Presentation type：Poster presentation  

Venue：大阪大学吹田キャンパス (吹田市)  

CiNii Research

Event date： 2000.6

Language：English   Presentation type：Poster presentation  

Venue：大宮ソニックシティ (大宮市)  

CiNii Research

Event date： 1999.9

Language：Japanese   Presentation type：Poster presentation  

Venue：日本歯科大学 (東京都千代田区)  

CiNii Research

Event date： 1999.9

Language：Japanese   Presentation type：Poster presentation  

Venue：日本歯科大学 (東京都千代田区)  

CiNii Research

Language：Japanese  

Language：English  

Language：English  

Language：Japanese  

Language：English  

Language：Japanese