著者

ラーマン ムスタフィジュー 山村 健介 井上 誠 黒瀬 雅之 山田 好秋

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日本生理学会

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vol.2005, pp.S172, 2005

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Previous studies have shown that the jaw-opening reflex (JOR) is modulated during mastication. However in these studies, analyses have been carried out for limited period within the masticatory sequence (i.e. from food intake to just before swallow). Our aim is to study if the modulatory pattern of the JOR is consistent throughout the masticatory sequence in awake rabbits. The masticatory sequence was divided into three masticatory periods (preparatory, rhythmic-chewing and preswallow periods) based on the jaw movement patterns and the activity pattern of the jaw muscles. Electromyographic activity of the jaw-opening muscle (Digastric) and the jaw movement trajectories were recorded. Repetitive electrical stimulation (single pulse, 0.2 ms duration at a rate of 1 Hz, 1.2 times the threshold) of the inferior alveolar nerve was conducted before (for control response) and during mastication to evoke the JOR. The amplitude of the JOR was normalized to the control response and the modulatory pattern of the JOR was compared among the masticatory periods. The JOR was generally suppressed during the rhythmic-chewing and the preswallow periods; the suppressive effect was phasically weakened in the middle part of the jaw opening during the rhythmic-chewing period. On the other hand, the reflex was not only suppressed but also facilitated during the preparatory period. The results suggest that the modulatory pattern of the jaw-opening reflex is different among the masticatory periods. <b>[Jpn J Physiol 55 Suppl:S172 (2005)]</b>

著者

余 錦 佐藤 純 舟久保 恵美 小畑 光央 水村 和枝

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日本生理学会

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vol.2004, pp.S245, 2004

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To examine the effects of change in meteorological factors on autonomic parameters in conscious animals, male Sprague-Dawley rats (n = 11) were exposed to lowering barometric pressure (LP) in a climate-controlled room. Systemic blood pressure (BP) was telemetrically recorded using a radio-transmitter equipped with a BP transducer. Heart rate (HR) was calculated from BP data and pulse interval variability was analyzed by power spectrograms obtained by the fast-Fourier transform algorithm. The low-frequency (LF: 0.02-0.6 Hz) power, high-frequency (HF: 0.8-3.0 Hz) power and LF/HF ratio, an index of relative sympathetic activity, were calculated. The rats were exposed to LP by decreasing the barometric pressure of the room by 27 hPa lower than the atmospheric pressure. This was done over 8 min. The pressure was maintained at this level for 29 min, and then returned to the baseline pressure over 8 min. The BP markedly increased after reaching the pre-set low pressure and reached the peak value at the middle of LP-exposure period. The HR and LF/HF ratio clearly rose in the early part of the LP-exposure period and then gradually decreased to the level before exposure. The LF/HF ratio also transiently increased at the recompression period. These results show that lowering barometric pressure within the range of natural environmental fluctuation induces autonomic responses in conscious rats. The increase in the LF/HF ratio during LP exposure indicates that low pressure environment induces sympathetic > parasympathetic activation. <b>[Jpn J Physiol 54 Suppl:S245 (2004)]</b>

著者

白 云哲 奥村 敏 常松 尚志 焦 其彬 小野 伸二 鈴木 さやか 黒谷 玲子 佐藤 元彦 南沢 享 石川 義弘

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日本生理学会

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vol.2008, pp.180-180, 2008

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Objective: Autonomic nervous activity is altered under microgravity. Cardiac response to autonomic regulation is mostly determined by &beta;-adrenergic receptors/cAMP signal that is regulated by adenylyl cyclase (AC). We thus examined the role of a major cardiac AC isoform, type 5 AC (AC5), in the autonomic regulation of the heart under microgravity induced by parabolic flights. Methods: We used transgenic mice with either disrupted (AC5KO) or overexpressed AC5 in the heart (AC5TG), and analyzed heart rate variability during parabolic flight. Results: The standard deviation of normal R-R intervals, a marker of total autonomic variability, was significantly greater under microgravity in AC5KO while no significant changes in WT and AC5TG. LF (low frequency)/HF (high frequency), a marker of sympathetic activity, became significantly lower under microgravity in WT and AC5TG while there was no such a decrease in AC5KO. Normalized HF, a marker of parasympathetic activity, became significantly greater in WT under microgravity, and became even greater in AC5TG, while no such increase in AC5KO. Conclusions: Putting together, changes in autonomic indexes in response to microgravity were augmented in AC5TG while attenuated in AC5KO, suggesting that AC5 plays a major role in determining the magnitude of cardiac responses to autonomic regulation under microgravity. <b>[J Physiol Sci. 2008;58 Suppl:S180]</b>

著者

グロス コーネリアス

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日本生理学会

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vol.2008, pp.2, 2008

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People who suffer from anxiety tend to interpret ambiguous situations, situations that could potentially be dangerous but not necessarily so, as threatening. It is also recognized that a person's propensity for anxiety can be influenced by early life experiences. We have shown that signaling by the neurotransmitter serotonin during early postnatal development in the mouse is about to moderate life-long anxiety behavior. Specifically, genetic or pharmacological blockade of the serotonin 1A receptor (Htr1aKO) during this period leads to increased anxiety both to innate anxiety cues (exposure novel arena) as well as enhanced fear conditioning to ambiguous, but not non-ambiguous conditioned stimuli. To examine the involvement of specific forebrain circuits in this phenotype, we developed a pharmacogenetic technique for the rapid tissue and cell-type specific silencing of neural activity in vivo. Inhibition of neurons in the central nucleus of the amygdala suppressed conditioned responses to both ambiguous and non-ambiguous cues. In contrast, inhibition of hippocampal dentate gyrus granule cells selectively suppressed conditioned responses to ambiguous cues and reversed the Htr1aKO phenotype. These data demonstrate that Htr1aKO mice have a bias in the processing of threatening cues that is moderated by hippocampal mossy fiber circuits and suggest that the hippocampus plays an important role in the response to ambiguous aversive stimuli. <b>[J Physiol Sci. 2008;58 Suppl:S2]</b>

著者

シュウ ワッシ

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日本生理学会

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vol.2006, pp.35, 2006

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Alzheimer's disease (AD), the most common form of senile dementia, is characterized by excessive production and accumulation of neurotoxic &beta;-amyloid (A&beta;) peptides which are proteolytically derived from &beta;-amyloid precursor protein (APP) via &beta;- and &gamma;-secretase cleavages. Experimental evidence from several groups including our own has demonstrated that the production of A&beta; occurs largely in the trans-Golgi network (TGN) where APP molecules predominantly reside. Mutations in presenilins genes are associated with the majority of familial AD likely through a mechanism of increase A&beta;42 production. Presenilins (PS, PS1 and PS2) along with their associated proteins including nicastrin (Nct), PEN2 and APH1 are essential for the &gamma;-secretase activity. The precise functions of Nct, APH-1 and PEN-2 have not been fully elucidated. Recent studies including ours suggest that PEN-2 mediates endoproteolysis of PS1, while APH-1 and Nct play regulatory roles in maintaining the stability of PS1 and the complex. PS1 knockout mice exhibit pre-neonatal lethality and PS1 has also been shown to affect numerous physiological functions including calcium homeostasis, skeletal development, neurite outgrowth, apoptosis, synaptic plasticity, tumorigenesis. These data strongly indicate critical physiological roles of PS1 addition to its essential role in &gamma;-secretase activity. We and others have reported that PS1 plays an important role in intracellular trafficking (especially from the TGN to the plasma membrane) of select membrane proteins including APP, PEN2 and nicastrin. The detailed cell biological mechanism for PS-mediated protein trafficking will be discussed. <b>[J Physiol Sci. 2006;56 Suppl:S35]</b>

著者

武田 紗路 藤井 陽平 ウェチュレック ニーナ オッファマン ステファン 坪川 宏

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PHYSIOLOGICAL SOCIETY OF JAPAN

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pp.153, 2007 (Released:2007-07-10)

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Although electrical properties of the dendrites are going to be clarifying, little is known about the physiological roles of dendritic spike. Since spike backpropagation could depolarize the inhibitory postsynapses, it may induce transient suppression of GABAergic inhibition (DSI) through an activation of presynaptic cannabinoid receptor (CBR). In this study, we examined whether action potentials induce DSI in mouse hippocampal neurons. Whole-cell voltage-clamp or current-clamp recording was made from the soma and/or the dendrite of CA1 neurons, and changes in amplitude of IPSCs (or IPSPs) after antidromic action potentials were analyzed. We found that train of antidromic spikes could induce transient suppression of GABAergic IPSCs (or IPSPs), which have CBR-dependent and TEA-sensitive components. However, depolarization by current injection to the dendrite failed to induce CBR-dependent suppression, indicating that somatic depolarization was required. In the presence of TEA, application of phorbol ester, which facilitates spike backpropagation, enhanced DSI, and application of somatostatine, which inhibits backpropagation, reduced DSI. These results suggest that in physiological condition antidromic invasion of Na+ spikes into dendrites induce DSI in hippocampal GABAergic synapses. Supported by a grant from Japanese Ministry of Education, Science, Sports and Culture (to H.T). [J Physiol Sci. 2007;57 Suppl:S153]

著者

田原 優 平尾 彰子 坪井 琢磨 田中 麻貴 吉田 晶子 柴田 重信

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日本生理学会

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vol.2008, pp.90, 2008

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Glycine is now used as a chemical for promotion of sleep in humans. It has been demonstrated that glycine administration up to 2g/kg causes the increase of NREM sleep in sleep disturbed rat and hypothermia (0.6 C decrease) in rat. The administration of benzodiazepine not only caused the sleep but affected the circadian rhythm; it blocked the light-induced phase advance of activity rhythm and elevation of Per1 gene expression in the suprachiasmatic nucleus (SCN) in hamsters. In the present experiment, we examined the possibility whether glycine affect light-induced phase shift and c-fos expression in the SCN and retina of mice. Glycine dose-dependently decreased the body temperature of mice (1C decrease with 2 g/kg). After extended light exposure for 2 hrs in the night under LD cycle mouse was kept under constant dark condition. Glycine (0.5-2 g/kg) pretreatment before light exposure dose-dependently attenuated light-induced phase delay. Glycine (2g/kg) pretreatment slightly attenuated light-induced increase of Fos immunoreactivity in the mouse SCN. Further experiment should elucidate whether glycine administration itself causes the phase shift or not. The present results suggest that high dose of glycine may attenuate the light-induced phase shift of circadian clock. <b>[J Physiol Sci. 2008;58 Suppl:S90]</b>

著者

平尾 彰子 田原 優 井筒 裕之 本間 さと 本間 研一 柴田 重信

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日本生理学会

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vol.2008, pp.198, 2008

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Daily restricted feeding (RF) with fixed time during daytime causes an advance of circadian rhythm of mouse liver clock gene expression. However, the mechanism of entrainment signal is poorly understood. Here, we examine whether daily administration of various type of nutrition caused entrainment of liver clock gene expression rhythm using Bmal1-luciferase transgenic mouse. Circadian rhythm change of liver bioluminescence was recorded through Lumicycle after 1-6 days of administration of various nutrients. We administered the corn carbon dehydrate, egg albumin or soybean oil after adjustment of each calorie. Among these nutrients soybean oil has most strong effect on phase-shift of gene expression rhythm. Administration of glucose through oral or intraperitoneal caused the phase advance, however the value of change was small. Thus, slow supply of calorie may be important to cause phase shift. We still examine the other nutrients such as amino acids, dextrin and sugar. We also try to find the effect of combination of nutrients on phase-shift of liver clock. <b>[J Physiol Sci. 2008;58 Suppl:S198]</b>

著者

松井 等 松井 等 高井 章 柏柳 誠

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PHYSIOLOGICAL SOCIETY OF JAPAN

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pp.S123, 2005 (Released:2005-04-16)

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In olfactory receptor cells, it is well established that cAMP acts as a main second messenger during odor responses. Biochemical experiments, however, showed failure of accumulation of cAMP in olfactory cilia by odorants of 40% examined (Sklar et al., 1996). We have shown that application of water soluble odorants and volatile odorants induced inward currents in olfactory cells of the Xenopus water nose but dialysis with cAMP did not (Iida and Kashiwayanagi, 1999). Breer and Boekhoff showed that odorants, which did not induce cAMP accumulation in olfactory cilia, induced IP3 accumulation (1990). Dialysis of olfactory cells in Xenopus water nose with IP3 induced inward currents. In addition, the turtle olfactory cells responded to dialysis with cyclic ADP-ribose (cADPR) with an inward current (Sekimoto and Kashiwayanagi, 2003). The magnitudes of the inward current responses to cAMP-increasing odorants were greatly reduced by prior dialyses of a high concentration of cADPR or 8-Br-cADPR, an antagonist. It is possible that IP3 and cADPR play as second messengers during the olfactory transduction. At present, channel molecules which are activated by these second messenger candidates have not been identified in olfactory cells. Transient receptor potential (TRP) channels, which are expressed in many tissues and cell types in vertebrates, are activated by various stimulations. In the present study, we explore roles of TRP channels in the olfactory system by RT-PCR and immunohistochemical techniques. [Jpn J Physiol 55 Suppl:S123 (2005)]

著者

石井 久淑 新岡 丈治 和泉 博之

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日本生理学会

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vol.2006, pp.202-202, 2006

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The sympathetic nerve (SN) has been reported to be involved in the development of jaw muscle dysfunctions because the masseter muscle pain is usually accompanied with the increase in the SN activity. We have recently reported that there are parasympathetic (PS) vasodilator fibers in the rat masseter muscle and that these fibers would be involved in the regulation of the hemodynamics of jaw muscles (J. Physiol. 569, 617-629, 2005). It is still unclear whether there is an interaction between the PS vasodilatation (PSV) in the masseter muscle and the SN activity. The present study was thus designed to examine 1) the effect of SN activation on the PSV in the masseter muscle, and 2) the neural mechanisms mediating the effect in anesthetized rats. The PS mediated masseter muscle blood flow (MBF) increases were evoked by electrical stimulation of the central cut end of the lingual nerve. The magnitudes of MBF increase were significantly reduced by ongoing electrical stimulation of the superior cervical sympathetic trunk in a frequency-dependent manner (0.5-10 Hz). Pretreatment with BIBP 3226, a neuropeptide Y (NPY) Y1 receptor antagonist, significantly reduced 30-40% in this inhibition, but phentolamine had no effect. The present study indicates that the excessive SN activation inhibits the PSV in the masseter muscle, suggesting a potential role in the etiology of jaw muscle dysfunctions. This inhibitory action may be due to an interaction of the PS vsodilator fibers and NPY that would be released from sympathetic fibers. <b>[J Physiol Sci. 2006;56 Suppl:S202]</b>

著者

美藤 純弘 藤井 昭仁 舩橋 誠 小橋 基 松尾 龍二

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日本生理学会

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vol.2007, pp.236-236, 2007

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We showed the glutamatergic, GABAergic and glycinergic synaptic inputs to superior salivatory (SS) neurons which is the primary center of submandibular salivary secretion. This glutamatergic input is considered to derive from the forebrain and brainstem. In the present study, we studied how SS neurons receive the glutamatergic inputs from the forebrain and brainstem in rats. The SS neurons innervating the salivary glands were labeled by retrograde axonal transport of a fluorescent dye. Subsequently some rats were decerebrate. Whole-cell patch-clamp recordings were performed from the labeled cells in slices. Excitatory postsynaptic currents were evoked by electrical stimulation near the recording cell. As compared with normal SS neurons, decerebrate SS neurons showed 3 types of the responses: enhanced responses, similar responses, no responses. The SS neurons which showed enhanced EPSCs receive the excitatory inputs from forebrain and brainstem. Decerebration induced denervation-hypersensitivity in the glutamate receptors. Enhanced EPSCs may be evoked by stimulation of glutamatergic inputs from brainstem. The SS neurons displayed similar responses have mainly excitatory inputs from the brainstem. The SS neurons which displayed no responses produced larger currents by the application of glutamate, suggesting that this type has excitatory inputs exclusively from the forebrain. <b>[J Physiol Sci. 2007;57 Suppl:S236]</b>