記述言語：英語   掲載種別：研究論文（学術雑誌）  

In this study, we determined whether the 201Tl (thallium-201)-based olfactory imaging is affected if olfactory sensory neurons received reduced pre-synaptic inhibition signals from dopaminergic interneurons in the olfactory bulb in vivo. The thallium-201 migration rate to the olfactory bulb and the number of action potentials of olfactory sensory neurons were assessed 3 h following left side nasal administration of rotenone, a mitochondrial respiratory chain complex I inhibitor that decreases the number of dopaminergic interneurons without damaging the olfactory sensory neurons in the olfactory bulb, in mice (6-7 animals per group). The migration rate of thallium-201 to the olfactory bulb was significantly increased following intranasal administration of thallium-201 and rotenone (10 μg rotenone, p = 0.0012; 20 μg rotenone, p = 0.0012), compared with that in control mice. The number of action potentials was significantly reduced in the olfactory sensory neurons in the rotenone treated side of 20 μg rotenone-treated mice, compared with that in control mice (p = 0.0029). The migration rate of thallium-201 to the olfactory bulb assessed with SPECT-CT was significantly increased in rats 24 h after the left intranasal administration of thallium-201 and 100 μg rotenone, compared with that in control rats (p = 0.008, 5 rats per group). Our results suggest that thallium-201 migration to the olfactory bulb is increased in intact olfactory sensory neurons with reduced pre-synaptic inhibition from dopaminergic interneurons in olfactory bulb glomeruli.

DOI： 10.1007/s12035-020-02078-y

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The parallel processing of chemical signals by the main olfactory system and the vomeronasal system has been known to control animal behavior. The physiological significance of peripheral parallel pathways consisting of olfactory sensory neurons and vomeronasal sensory neurons is not well understood. Here, we show complementary characteristics of the information transfer of the olfactory sensory neurons and vomeronasal sensory neurons. A difference in excitability between the sensory neurons was revealed by patch-clamp experiments. The olfactory and vomeronasal sensory neurons showed phasic and tonic firing, respectively. Intrinsic channel kinetics determining firing patterns was demonstrated by a Hodgkin-Huxley-style computation. Our estimation of the information carried by action potentials during one cycle of sinusoidal stimulation with variable durations revealed distinct characteristics of information transfer between the sensory neurons. Phasic firing of the olfactory sensory neurons was suitable to carry information about rapid changes in a shorter cycle (<200 ms). In contrast, tonic firing of the vomeronasal sensory neurons was able to convey information about smaller stimuli changing slowly with longer cycles (>500 ms). Thus, the parallel pathways of the two types of sensory neurons can convey information about a wide range of dynamic stimuli. A combination of complementary characteristics of olfactory information transfer may enhance the synergy of the interaction between the main olfactory system and the vomeronasal system.

DOI： 10.1016/j.neuroscience.2018.12.043

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier B.V.  

Anxiety- and stress-related disorders can be debilitating psychiatric conditions in humans. To prevent or ameliorate these conditions, reliable animal models are needed to evaluate the effects of anxiolytic drugs. Previously, we found that a mixture of three pyrazine analogues (P-mix) that were present at high levels in wolf urine induced fear-related responses in mice, rats and deer. A change in cutaneous temperature was shown to be induced by acute stress simultaneously with changes in heart rate, arterial pressure and freezing behavior, raising the possibility that cutaneous temperature could be used as an index of stress. In the present study, using infrared thermography, we showed that exposure of mice to P-mix induced a decrease in cutaneous temperature. We then examined the dose-dependent effects of an anxiolytic drug, etizolam (0–20 mg/kg), on the temperature decrease. Pre-administration of etizolam (5 mg/kg or higher) inhibited the P-mix-induced decrease in cutaneous temperature. Exposure to P-mix induced Fos-immunoreactivity, a marker of neuronal excitation, at the mouse amygdala and hypothalamus, and etizolam (5 mg/kg) attenuated that immunoreactivity. The present results suggested that the measurement of cutaneous P-mix-induced temperature changes in mice could be used as an animal model for evaluating the effects of anxiolytic drugs.

DOI： 10.1016/j.ejphar.2018.02.015

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：PERGAMON-ELSEVIER SCIENCE LTD  

(Objective) The subventricular zone in mice generates a lot of neuroblasts even during adulthood. These neuroblasts migrate to the olfactory bulb and differentiate into inhibitory interneurons such as granule cells and periglomerular cells. Olfactory sensory neurons receive information from various odorants and transmit it to the olfactory bulb. Our previous study showed that soft-diet feeding impairs neurogenesis in the subventricular zone, in turn leading to the reduction of odor-induced behaviors and Fos-immunoreactivities, the latter of which are markers of neural activity, at the olfactory bulb after exposure to odors. Release of GABA from inhibitory interneurons at the olfactory bulb induces inhibitory currents at the mitral cells, which are output neurons from the olfactory bulb. (Design) In the present study, we measured spontaneous inhibitory postsynaptic currents (sIPSCs) at the mitral cells of mice fed a soft diet in order to explore the effects of changes in texture of diets on neural function at the olfactory bulb. (Results) The soft-diet feeding extended the intervals between sIPSCs and reduced their peak amplitudes. (Conclusions) The present results suggest that soft-diet feeding in mice attenuates the neural functions of inhibitory interneurons at the olfactory bulb.

DOI： 10.1016/j.archoralbio.2017.07.015

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：PHARMACEUTICAL SOC JAPAN  

Exposure to environmental neurotoxins is suspected to be a risk factor for sporadic progressive neurodegenerative diseases. Parkinson's disease has been associated with exposure to the pesticide rotenone, a mitochondrial respiration inhibitor. We previously reported that intranasal administration of rotenone in mice induced dopaminergic (DA) neurodegeneration in the olfactory bulb (OB) and reduced olfactory functions. In the present study, we investigated the DA neurons in the brains of mice that were administered rotenone intranasally for an extended period. We found that the olfactory function of mice was attenuated by rotenone administration. Electrophysiological analysis of the mitral cells, which are output neurons in the OB, revealed that the inhibitory input into the mitral cells was retarded. In the immunohistochemical analysis, neurite degeneration of DA neurons in the substantia nigra was observed in rotenone -administered mice, indicating that rotenone progressively initiated the degeneration of cerebral DA neurons via the nasal route.

DOI： 10.1248/bpb.b16-00654

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE BV  

Many environmental chemicals are thought to affect brain function. It was reported that chemicals-in the nasal cavity directly reach the brain through the connection between olfactory neurons and the olfactory bulb (OB). In this 'olfactory transport,' xenobiotics absorbed at the nasal mucosa reach the brain by bypassing some physical barriers and defenses, and thus olfactory transport is suspected to be a vulnerable mechanism of the brain against invasion threats of environmental chemicals. In this study, we focused on the neuronal toxicity of rotenone administered intranasally to mice. The results showed that the mice that were administered rotenone had attenuated olfactory functions. We also found that intranasally administered rotenone induced acute mitochondrial stress at the OB. The repeated administration of rotenone resulted in a decrease in the number of dopaminergic neurons, which are inhibitory interneurons in the OB. Taken together, our findings suggest that the inhalation of environmental toxins induces the neurodegeneration of cranial neurons through olfactory transport, and that olfactory dysfunction may be induced as an earliest symptom of neurodegeneration caused by inhaled neurotoxins. (C) 2015 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.neuro.2015.10.006

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：PHARMACEUTICAL SOC JAPAN  

TRPV2, a member of the transient receptor potential family, has been isolated as a capsaicin-receptor homolog and is thought to respond to noxious heat. Here we show that TRPV2 mRNA is predominantly expressed in the subpopulation of olfactory sensory neurons (OSNs). We carried out histochemical analyses of TRPV2 and insulin-like growth factor-I receptor (IGF-IR) using in situ hybridization and immunofluorescence in the adult olfactory system. In olfactory mucosa, intensive TRPV2 immunostaining was observed at the olfactory axon bundles but not at the soma. TRPV2-positive labeling was preferentially found in the olfactory nerve layer in the olfactory bulb (OB). Furthermore, we demonstrated that a positive signal for IGF-IR mRNA was detected in OSNs expressing TRPV2 mRNA. In embryonic stages, TRPV2 immunoreactivity was observed on axon bundles of developing OSNs in the nasal region starting from 12.5d of gestation and through fetal development. Observations in this study suggest that TRPV2 coupled with IGF-IR localizes to growing olfactory axons in the OSNs.

DOI： 10.1248/bpb.b14-00413

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER IRELAND LTD  

Recently, evidence has accumulated that the vomeronasal system cooperates with the main olfactory system to process volatile cues that regulate the animal's behavior. This is contradictory to the traditional view that the vomeronasal system is quite different from the main olfactory system in the time scale of information processing. Particularly, the firing rate of mitral/tufted cells in the accessory olfactory bulb (MTAOB) is known to be significantly lower than that of mitral cells in the main olfactory bulb (MCMOB). To address this question of whether the low-frequency firing in MTAOB carries less information than the high-frequency firing in MCMOB in the early stages of stimulation, we compared MTAOB and MCMOB for their firing mechanisms and information transfer characteristics. A model computation demonstrated that the inherent channel kinetics of MTAOB was responsible for their firing at a lower frequency than MCMOB. Nevertheless, our analysis suggested that MTAOB were comparable to MCMOB in both the amount and speed of information transfer about depolarizing current intensity immediately after current injection onset (&lt;200 ms). Our results support a hypothesis of simultaneous processing of common cues in both systems. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.neulet.2014.05.058

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：PUBLIC LIBRARY SCIENCE  

The subventricular zone (SVZ) generates an immense number of neurons even during adulthood. These neurons migrate to the olfactory bulb (OB) and differentiate into granule cells and periglomerular cells. The information broadcast by general odorants is received by the olfactory sensory neurons and transmitted to the OB. Recent studies have shown that a reduction of mastication impairs both neurogenesis in the hippocampus and brain functions. To examine these effects, we first measured the difference in Fos-immunoreactivity (Fos-ir) at the principal sensory trigeminal nucleus (Pr5), which receives intraoral touch information via the trigeminal nerve, when female adult mice ingested a hard or soft diet to explore whether soft-diet feeding could mimic impaired mastication. Ingestion of a hard diet induced greater expression of Fos-ir cells at the Pr5 than did a soft diet or no diet. Bromodeoxyuridine-immunoreactive (BrdU-ir) structures in sagittal sections of the SVZ and in the OB of mice fed a soft or hard diet were studied to explore the effects of changes in mastication on newly generated neurons. After 1 month, the density of BrdU-ir cells in the SVZ and OB was lower in the soft-diet-fed mice than in the hard-diet-fed mice. The odor preferences of individual female mice to butyric acid were tested in a Y-maze apparatus. Avoidance of butyric acid was reduced by the soft-diet feeding. We then explored the effects of the hard-diet feeding on olfactory functions and neurogenesis in the SVZ of mice impaired by soft-diet feeding. At 3 months of hard-diet feeding, avoidance of butyric acid was reversed and responses to odors and neurogenesis were recovered in the SVZ. The present results suggest that feeding with a hard diet improves neurogenesis in the SVZ, which in turn enhances olfactory function at the OB.

DOI： 10.1371/journal.pone.0097309

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記述言語：日本語   出版者・発行元：(一社)日本鼻科学会  

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

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担当区分：筆頭著者   記述言語：日本語   掲載種別：研究論文（大学，研究機関等紀要）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：PHARMACEUTICAL SOC JAPAN  

Cremophor EL (CrEL) is a non-Ionic surfactant widely used as a vehicle for Insoluble drugs, including immunosuppressive and anticancer agents Although CrEL has often been reported to Induce sensory neuropathies, its action on voltage-gated ion channels remains unknown We show here that CrEL modulates voltage-gated sodium current (INa) and potassium current (IK) of human neuroblastoma cells (SH-SY5Y) First, CrEL suppressed the amplitude of INa and that of IK The suppression-concentration curve for INa was gradual but that for IK was steeper, indicating that INa remains Incompletely blocked by high concentrations of CrEL, which greatly reduce IK Thus, it is possible that CrEL paradoxically increases neuronal excitability at higher concentrations Next, CrEL accelerated IK's inactivation process The voltage-dependent inactivation of IK showed two time constants, tau(f) of 322 +/- 49 ms and tau(s) of 2925 +/- 184 ms, under the control condition By applying 1000 ppm CrEL, three time constants-tau(u) of 23 +/- 2 ms, tau(f) of 196 +/- 19 ms, and tau(s) of 1396 +/- 127 ms-appeared in the inactivation process This modified inactivation of IK probably disturbs the repolarizing phases of action potentials These modulations of voltage-gated ion channels by CrEL may cause abnormal excitability involved in neuropathies

DOI： 10.1248/bpb.33.2013

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記述言語：日本語   掲載種別：研究論文（学術雑誌）  

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記述言語：英語   掲載種別：研究論文（国際会議プロシーディングス）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

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担当区分：筆頭著者   記述言語：日本語   掲載種別：研究論文（大学，研究機関等紀要）  

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記述言語：英語   掲載種別：研究論文（国際会議プロシーディングス）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

The Kv4.2 transient voltage-dependent potassium current contributes to the morphology of the cardiac action potential as well as to neuronal excitability and firing frequency. Here we report profound effects of the Kv4.2 C terminus on the surface expression and activation gating properties of Kv4.2 that are modulated by the direct interaction between KChIP2, an auxiliary regulatory subunit, and the C terminus of Kv4.2. We show that increasingly large truncations of the C terminus of rat Kv4.2 (wild type) cause a progressive decrease of Kv4.2 current along with a shift in voltage-dependent activation that is closely correlated with negative charge deletion. Co-expression of more limited Kv4.2 C-terminal truncation mutants (T588 and T528) with KChIP2 results in a doubling of Kv4.2 protein expression and up to an 8-fold increase in Kv4.2 current amplitude. Pulse-chase experiments show that co-expression with KChIP2 slows Kv4.2 wild type degradation 8-fold. Co-expression of KChIP2 with an intermediate-length C-terminal truncation mutant (T474) shifts Kv4.2 activation voltage dependence and enhances expression of Kv4.2 current. The largest truncation mutants (T417 and Delta C) show an intracellular localization with no measurable currents and no response to KChIP2 co-expression. Co-immunoprecipitation and competitive glutathione S-transferase-binding assays indicate a direct interaction between KChIP2 and the Kv4.2 C terminus with a relative binding affinity comparable with that of the N terminus. Overall, these results suggest that the C-terminal domain of Kv4.2 plays a critical role in voltage-dependent activation and functional expression that is mediated by direct interaction between the Kv4.2 C terminus and KChIP2.

DOI： 10.1074/jbc.M604843200

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：COMPANY OF BIOLOGISTS LTD  

Mutations of a putative cyclic-nucleotide-binding domain (CNBD) can disrupt the function of the hyperpolarization-activated cyclic-nucleotide-gated channel (HCN2) and the human ether-a-go-go-related gene potassium channel (HERG). Loss of function caused by C-terminal truncation, which includes all or part of the CNBD in HCN and HERG, has been related to abnormal channel trafficking. Similar defects have been reported for several of the missense mutations of HERG associated with long QT syndrome type 2 (LQT2). Thus, we postulate that normal processing of these channels depends upon the presence of the CNBD. Here, we show that removal of the entire CNBD prevents Golgi transit, surface localization and function of HERG channel tetramers. This is also true when any of the structural motifs of the CNBD is deleted, suggesting that deletion of any highly conserved region along the entire length of the CNBD can disrupt channel trafficking. Furthermore, we demonstrate that defective trafficking is a consequence of all LQT2 mutations in the CNBD, including two mutations not previously assessed and two others for which there are conflicting results in the literature. The trafficking sensitivity of the CNBD might be of general significance for other ion channels because complete deletion of the CNBD or mutations at highly conserved residues within the CNBD of the related ERG3 channel and HCN2 also prevent Golgi transit. These results broadly implicate the CNBD in ion-channel trafficking that accounts for the commonly observed loss of function associated with CNBD mutants and provides a rationale for distinct genetic disorders.

DOI： 10.1242/jcs.02423

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記述言語：英語   掲載種別：研究論文（国際会議プロシーディングス）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE BV  

Taste bud cells (TBCs) on soft palates differ from those on tongues in innervation and chemosensitivity. We investigated voltage-gated channels involved in the taste responses of TBCs on mouse soft palates under in-situ tight-seal voltage/current-clamp conditions. Under the cell-attached mode, TBCs spontaneously fired action currents, which were blocked by application of 1 muM TTX to TBC basolateral membranes. Firing frequencies increased in response to taste substances applied to TBC receptor membranes. Under the whole-cell clamp mode, as expected, TBCs produced various voltage-gated currents such as TTX-sensitive Na+ currents (I-Na), outward currents (I-out) including TEA-sensitive and insensitive currents, inward rectifier K+ currents (I-ir), and Ca2+ currents including T-type, P/Q-type, and L-type Ca2+ currents. We classified TBCs into three types based on the magnitude of their voltage-gated Na+ currents and membrane capacitance. HEX type (60% of TBCs examined) was significantly larger in Na+ current magnitude and smaller in membrane capacitance than LEX type (23%). NEX type (17%) had no Na+ currents. HEX type was equally distributed within single taste buds, while LEX type was centrally distributed, and NEX type was peripherally distributed. There were correlations between these electrophysiological cell types and morphological cell types determined by three-dimensional reconstruction. The present results show that soft palate taste buds contain TBCs with different electrophysiological properties, and suggest that their co-operation is required in taste transduction. (C) 2003 Elsevier B.V. All rights reserved.

DOI： 10.1016/S0006-8993(03)03013-0

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Wiley-Liss Inc.  

We investigated the blocking effect of the conformationally restricted analogs of milnacipran on NMDA receptors by recording the whole-cell currents of Xenopus oocytes injected with rat brain mRNA and the single channel currents of cultured hippocampal neurons under voltage-clamp conditions. Their protective effect against excitotoxicity was also investigated on cultured cortex neurons. All conformationally restricted analogs examined blocked activated NMDA receptors, though their structures were quite different from known Nmda receptor blockers. The analogs with a (1S, 2R, 1'S)-configuration such as PPDC ((1S, 2R)-1-phenyl-2 [(S)-1-aminopropyl]- N,N-diethylcyclopropanecarboxamide) had lower IC50 values than those with other configurations. The empirical Hill coefficients for each compound were close to unity, indicating a 1:1 stoichiometry for the block. Ppdc decreased the maximum responses to both N-methyl D-aspartate (nmda) and glycine without altering their dissociation constants. The blocking effect was enhanced on hyperpolarization. Ppdc had no effects on other glutamate receptor subtypes (AMPA, kainate, and metabotropic glutamate receptors) or other neurotransmitter receptors (GABA(A), 5HT(2C), and ACh(M1) receptors) produced by the oocytes. PPDC decreased the mean open time of NMDA receptors without decreasing their elementary conductance. The microscopic blocking rate constant was 2.8 x 107 M-1s-1. The macroscopic unblocking rate constant of PPDC was much faster than that of MK-801. Only the analogs with the (1S, 2R, 1'S)-configuration protected the cultures against NMDA-induced neurotoxicity, though they failed to protect against kainate-induced neurotoxicity. These results show that conformationally restricted analogs, at least PPDC, selectively blocked open channels of NMDA receptors.

DOI： 10.1002/(SICI)1098-2396(199902)31:2<87::AID-SYN1>3.0.CO;2-H

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

We recently demonstrated that (±)-(Z)-2-(aminomethyl)-1-phenyl-N,N-diethylcyclopropanecarboxamide [milnacipran, (±)-1], an inhibitor of the reuptake of serotonin (5-HT), was a noncompetitive NMDA receptor antagonist. On the basis of the cyclopropane structure of (±)-1, conformationally restricted analogs with different stereochemistries, namely 1-phenyl-2-(1-aminoalkyl)-N,N-diethylcyclopropanecarboxamindes (2,3, ent-2, and ent-3), were designed and synthesized. Among these analogs, 2a, 2b, and 2f, with (1S,2R,1′S)-configuration, were more efficient than milnacipran as NMDA receptor antagonists
these compounds significantly inhibited the binding of [3H]MK-801 at IC50 = 0.35 ± 0.08, 0.20 ± 0.024, and 0.16 ± 0.02 μM, respectively, and blocked the response of voltage-clamped oocytes to NMDA, surpassing the effects of (±)-1. Although both the 1′-methyl analog 2a and the 1′-vinyl analog 2f, like (±)-1, strongly inhibited 5-HT uptake in vitro, the corresponding 1′-ethyl analog 2b was devoid of the inhibitory effect on 5-HT uptake, while it was about 30 times more potent as an NMDA receptor antagonist than (±)-1.

DOI： 10.1021/jm960495w

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担当区分：筆頭著者   記述言語：日本語   掲載種別：記事・総説・解説・論説等（商業誌、新聞、ウェブメディア）   出版者・発行元：（株）中外医学社  

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記述言語：日本語   出版者・発行元：(株)日本臨床社  

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記述言語：日本語   出版者・発行元：(一社)日本生理学会  

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記述言語：日本語   出版者・発行元：一般社団法人 日本生物物理学会  

DOI： 10.2142/biophys.57.023

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記述言語：日本語   出版者・発行元：(一社)日本生理学会  

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記述言語：日本語   出版者・発行元：(一社)日本生理学会  

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記述言語：日本語   出版者・発行元：(一社)日本生理学会  

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記述言語：日本語   出版者・発行元：(一社)日本生理学会  

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雑誌掲載版

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記述言語：日本語   出版者・発行元：(一社)日本生理学会  

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記述言語：日本語   出版者・発行元：旭川医科大学  

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記述言語：日本語   出版者・発行元：日本味と匂学会  

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記述言語：日本語   出版者・発行元：日本味と匂学会  

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記述言語：日本語   出版者・発行元：日本味と匂学会  

マウスを、固形飼料で飼育した群と、粉末飼料で飼育した群の2群に分け、1ヵ月、3ヵ月および6ヵ月間飼育し、咀嚼が脳室下層、Rostral Migratory Stream、嗅球、副嗅球および海馬歯状回の神経新生と嗅覚機能に与える影響について検討した。ブロモデオキシウリジン(BrdU)陽性細胞の発現を指標として解析した。固形飼料で飼育したマウスに比べ粉末飼料で飼育したマウスでは、1ヵ月で脳室下層においてBrdU陽性細胞数の有意な減少が認められた。海馬歯状回では3ヵ月、6ヵ月の飼育でBrdU陽性細胞数の有意な減少を認め、脳室下層の方が海馬より早く神経新生の減少が生じていた。粉末飼料で飼育したマウスでは、嗅球においてもBrdU陽性細胞の減少を示し、それに遅れて副嗅球でもBrdU陽性細胞の有意な減少がみられた。

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記述言語：日本語   出版者・発行元：(一社)日本生理学会  

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記述言語：日本語  

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記述言語：日本語   出版者・発行元：(公社)日本薬学会  

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記述言語：日本語   出版者・発行元：日本味と匂学会  

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開催年月日： 2022年6月 - 2022年7月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2022年3月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2021年9月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2021年9月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：オンライン  

抄録p13

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開催年月日： 2021年9月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：オンライン  

抄録p16

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開催年月日： 2021年3月

記述言語：日本語   会議種別：シンポジウム・ワークショップ パネル（公募）  

開催地：オンライン  

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開催年月日： 2020年10月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：オンライン  

P-058, abstracts p98 柏柳メモリアル

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開催年月日： 2019年9月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2019年3月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2018年10月

記述言語：英語   会議種別：ポスター発表  

開催地：埼玉  

P-098, abstracts p105

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開催年月日： 2018年10月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2017年9月

記述言語：英語   会議種別：ポスター発表  

開催地：神戸  

P-116, abstracts p127

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開催年月日： 2017年9月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2017年9月

記述言語：英語   会議種別：ポスター発表  

開催地：神戸  

P-089, abstracts p118

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開催年月日： 2016年6月

記述言語：英語   会議種別：ポスター発表  

開催地：横浜  

ISOT 2016 Program Book. 28, P1-013

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開催年月日： 2016年6月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2016年6月

記述言語：英語   会議種別：ポスター発表  

開催地：横浜  

ISOT 2016 Program Book. 37, P1-071

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開催年月日： 2016年3月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2015年9月

記述言語：英語   会議種別：ポスター発表  

開催地：岐阜  

P-122, abstracts p129

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開催年月日： 2015年9月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2015年4月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：旭川医科大学  

要旨集9p

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開催年月日： 2015年4月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：旭川医科大学  

要旨集1p

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開催年月日： 2014年10月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2014年10月

記述言語：英語   会議種別：ポスター発表  

開催地：清水  

P-146, abstracts p133

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開催年月日： 2014年9月

記述言語：英語   会議種別：ポスター発表  

開催地：Dijon, France  

P31, Abstracts p203

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開催年月日： 2014年3月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：室蘭  

要旨集4p

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開催年月日： 2014年3月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：室蘭  

要旨集5p

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開催年月日： 2013年9月

記述言語：英語   会議種別：ポスター発表  

開催地：Prague, Czech Republic  

D: Sensory and motor systems PI-D-99

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開催年月日： 2013年9月

記述言語：英語   会議種別：ポスター発表  

開催地：Prague, Czech Republic  

PI-D-100

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開催年月日： 2013年9月

記述言語：英語   会議種別：ポスター発表  

開催地：仙台  

P-112, 予稿集p127

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開催年月日： 2013年9月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2013年9月

記述言語：英語   会議種別：ポスター発表  

開催地：仙台  

P-106, 予稿集p124

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開催年月日： 2013年9月

記述言語：英語   会議種別：ポスター発表  

開催地：仙台  

P-111, 予稿集p126

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開催年月日： 2013年8月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：旭川  

抄録p10

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開催年月日： 2013年8月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：旭川  

抄録p10

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開催年月日： 2013年3月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：網走  

抄録p10

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開催年月日： 2013年3月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：網走  

抄録p7

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開催年月日： 2012年10月

記述言語：英語   会議種別：ポスター発表  

開催地：大阪  

予稿集p91

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開催年月日： 2012年10月

記述言語：英語   会議種別：ポスター発表  

開催地：大阪  

予稿集p93

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開催年月日： 2012年10月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2011年10月

記述言語：英語   会議種別：ポスター発表  

開催地：金沢  

予稿集p129

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開催年月日： 2011年10月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2011年10月

記述言語：英語   会議種別：ポスター発表  

開催地：金沢  

予稿集p125

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開催年月日： 2010年9月

記述言語：英語   会議種別：ポスター発表  

開催地：北九州  

予稿集p91

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開催年月日： 2010年3月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：札幌  

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開催年月日： 2009年9月

記述言語：日本語   会議種別：ポスター発表  

開催地：旭川  

予稿集p99

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開催年月日： 2009年9月

記述言語：日本語   会議種別：ポスター発表  

開催地：旭川  

予稿集p99

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開催年月日： 2009年7月 - 2009年8月

記述言語：英語   会議種別：ポスター発表  

開催地：Kyoto, Japan  

Program p56

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開催年月日： 2009年6月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：熊谷  

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開催年月日： 2008年9月

記述言語：日本語   会議種別：ポスター発表  

開催地：富山  

予稿集p121

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開催年月日： 2008年9月

記述言語：英語   会議種別：ポスター発表  

開催地：Portoroz, Slovenia  

Abstracts p83

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開催年月日： 2008年9月

記述言語：英語   会議種別：ポスター発表  

開催地：Portoroz, Slovenia  

Abstracts p65

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開催年月日： 2003年9月

記述言語：日本語   会議種別：ポスター発表  

開催地：函館  

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開催年月日： 2003年7月

記述言語：日本語   会議種別：ポスター発表  

開催地：名古屋  

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開催年月日： 2002年11月

記述言語：英語   会議種別：ポスター発表  

開催地：Orlando  

Presentation No. 355.13

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開催年月日： 2002年7月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：広島  

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開催年月日： 2002年7月

記述言語：日本語   会議種別：ポスター発表  

開催地：東京  

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開催年月日： 2001年11月

記述言語：英語   会議種別：ポスター発表  

開催地：San Diego  

287.6

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開催年月日： 2000年3月

記述言語：英語   会議種別：口頭発表（一般）  

開催地：東京  

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開催年月日： 1999年7月

記述言語：英語   会議種別：ポスター発表  

開催地：大阪  

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開催年月日： 1998年11月

記述言語：英語   会議種別：ポスター発表  

開催地：Los Angeles  

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開催年月日： 1998年9月

記述言語：日本語   会議種別：ポスター発表  

開催地：東京  

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開催年月日： 1996年11月

記述言語：英語   会議種別：ポスター発表  

開催地：Washington D.C.  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：シンポジウム・ワークショップ パネル（指名）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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