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

Cardiomyocytes possess a non-neuronal cardiac cholinergic system (NNCCS) regulated by a positive feedback system; however, its other regulatory mechanisms remain to be elucidated, which include the epigenetic control or regulation by the female sex steroid, estrogen. Here, the NNCCS was shown to possess a circadian rhythm; its activity was upregulated in the light-off phase via histone acetyltransferase (HAT) activity and downregulated in the light-on phase. Disrupting the circadian rhythm altered the physiological choline acetyltransferase (ChAT) expression pattern. The NNCCS circadian rhythm may be regulated by miR-345, independently of HAT, causing decreased cardiac ChAT expression. Murine cardiac ChAT expression and ACh contents were increased more in female hearts than in male hearts. This upregulation was downregulated by treatment with the estrogen receptor antagonist tamoxifen, and in contrast, estrogen reciprocally regulated cardiac miR-345 expression. These results suggest that the NNCCS is regulated by the circadian rhythm and is affected by sexual dimorphism.

DOI： 10.1007/s12265-017-9750-4

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DOI： 10.1007/s12265-017-9750-4

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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：PORTLAND PRESS LTD  

We previously developed cardiac ventricle-specific choline acetyltransferase (ChAT) gene-overexpressing transgenic mice (ChAT tgm), i.e. an in vivo model of the cardiac non-neuronal acetylcholine (NNA) system or non-neuronal cardiac cholinergic system (NNCCS). By using this murine model, we determined that this system was responsible for characteristics of resistance to ischaemia, or hypoxia, via the modulation of cellular energy metabolism and angiogenesis. In line with our previous study, neuronal ChAT-immunoreactivity in the ChAT tgm brains was not altered from that in the wild-type (WT) mice brains; in contrast, the ChAT tgm hearts were the organs with the highest expression of the ChAT transgene. ChAT tgm showed specific traits in a central nervous system (CNS) phenotype, including decreased response to restraint stress, less depressive-like and anxiety-like behaviours and anti-convulsive effects, all of which may benefit the heart. These phenotypes, induced by the activation of cardiac NNCCS, were dependent on the vagus nerve, because vagus nerve stimulation (VS) in WT mice also evoked phenotypes similar to those of ChAT tgm, which display higher vagus nerve discharge frequency; in contrast, lateral vagotomy attenuated these traits in ChAT tgm to levels observed in WT mice. Furthermore, ChAT tgm induced several biomarkers of VS responsible for anti-convulsive and anti-depressive-like effects. These results suggest that the augmentation of the NNCCS transduces an effective and beneficial signal to the afferent pathway, which mimics VS. Therefore, the present study supports our hypothesis that activation of the NNCCS modifies CNS to a more stress-resistant state through vagus nerve activity.

DOI： 10.1042/CS20160277

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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：MEDICAL ASSOC NIPPON MEDICAL SCH  

Corticotropin-releasing factor (CRF) in the medial prefrontal cortex (mPFC) is suggested to play an important role in mediating fear, anxiety, and depression. The results of the studies of the actions of CRF in the mPFC regarding anxiety-related behavior, however, seem contradictory. In one study, microinjection of CRF into the mPFC produced an increase in anxiety-related behavior on the elevated plus maze, whereas in another study CRF produced an anxiolytic-like effect. To test whether the different doses of CRF used in these experiments are responsible for the differing results, we examined the dose-dependent effects of CRF (0.015, 0.05, 0.15, 0.5, and 1.0 µg/0.5 µL/site) microinjected into the bilateral mPFC of male Wistar rats on anxiety-related behavior in the elevated plus maze. We found that microinjection of 0.05 µg CRF significantly decreased the number of open-arm entries, whereas 1.0 µg CRF significantly increased the time spent on the open arms. The results indicate that CRF has effects opposing anxiety-related behavior in the elevated plus maze: anxiety-related behavior at a lower dose and an anxiolytic-like effect at a higher dose.

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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  

To clarify the role of ghrelin and its receptor (GHS-R) in the regulatory mechanism of energy metabolism, we analyzed transgenic (Tg) rats expressing an antisense GHS-R mRNA under the control of the tyrosine hydroxylase (TH) promoter. Tg rats showed lower visceral fat weight and higher O(2) consumption, CO(2) production, rectal temperature, dark-period locomotor activity, brown adipose tissue (BAT) weight and uncoupling protein 1 expression compared with wild-type (WT) rats on a standard diet. A high-fat diet for 14days significantly increased body weight, visceral fat weight, and the sizes of white and brown adipocytes in WT rats but not in Tg rats compared with the corresponding standard-diet groups. Antisense GHS-R mRNA was expressed and GHS-R expression was reduced in TH-expressing cells of the vagal nodose ganglion in Tg rats. Ghrelin administered intravenously suppressed noradrenaline release in the BAT of WT rats, but not in Tg rats. These results suggest that ghrelin/GHS-R plays an important role in energy storage by modifying BAT function and locomotor activity. As our previous study showed that peripheral ghrelin-induced noradrenaline release suppression in BAT is blocked by vagotomy, the present findings also suggest that vagal afferents transmit the peripheral ghrelin signal to the sympathetic nervous system innervating BAT.

DOI： 10.1016/j.regpep.2009.11.010

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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：BIOSCIENTIFICA LTD  

To clarify the role of ghrelin in the regulatory mechanism of energy metabolism, we analyzed the effects of centrally and peripherally administered ghrelin on noradrenaline release in the brown adipose tissue (BAT) of rats using a microdialysis system. I.c.v. administration of ghrelin at a dose of 500 pmol suppressed noradrenaline release in BAT, and microinjection of ghrelin (50 pmol) into the paraventricular nucleus (PVN) or arcuate nucleus (ARC) of the hypothalamus also suppressed noradrenaline release in BAT. In addition, i.v. administered ghrelin (30 nmol) suppressed noradrenaline release in BAT, and this suppression was blocked by a vagotomy. Neither i.c.v. nor i.v. administration of des-acyl ghrelin, which does not bind to GH secretagogue receptor type 1a (GHS-R1a), affected noradrenaline release in BAT. These results indicate that ghrelin increases energy storage by suppressing the activity of the sympathetic nerve innervating BAT. It seems that the PVN and ARC, which express GHS-R1a, are the sites of action of ghrelin in the brain and that the action of peripheral ghrelin on the sympathetic nerve activity innervating BAT is mediated by the vagal nerve, which also expresses GHS-R1a.

DOI： 10.1677/JOE-08-0374

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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  

Nicotine is known to stimulate energy expenditure, although the precise mechanism is unclear. To clarify the involvement of corticotropin-releasing factor (CRF) in the mechanism by which nicotine increases energy expenditure, the effect of intraperitoneal injection of nicotine (0.1 or 0.5mg/kg) on the release of noradrenaline (NA), a stimulator of thermogenesis, in brown adipose tissue (BAT) important for energy expenditure was examined in rats. We also examined the effects of CRF receptor subtype antagonists on the nicotine-induced change in BAT NA release. Nicotine significantly increased BAT NA release at a dose of 0.5mg/kg, and the increase was completely blocked by antalarmin, a CRF type 1 receptor antagonist, but not by antisauvagine-30, a CRF type 2 receptor antagonist. These results suggest that nicotine increases energy expenditure by activating BAT function, and that CRF type 1 receptors are involved in the mechanism by which nicotine affects energy balance.

DOI： 10.1016/j.neulet.2009.03.054

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Anorexia nervosa is mostly seen in adolescent females, although the gender-differentiation mechanism is unclear. Corticotropin-releasing factor (CRF), a key peptide for stress responses such as inhibition of food intake, increases in arousal and locomotor activity, and gonadal dysfunction, is thought to be involved in the pathophysiology of anorexia nervosa. CRF in the paraventricular nucleus of the hypothalamus (PVN) and CRF in the central nucleus of the amygdala (CeA) are involved in the regulation of stress responses, and gender differences in CRF mRNA expression in these regions in response to various stressors are controversial. We therefore examined CRF gene expression in the PVN and CeA as well as corticotropin (ACTH) and corticosterone secretion in response to a 60-min period of electric footshock (FS) or psychological stress (PS) induced by a communication box in both male and female rats in proestrus or diestrus in an effort to elucidate the mechanism underlying the gender difference in the activity of the hypothalamic-pituitary-adrenal (HPA) axis and the mechanism underlying the remarkable prevalence of anorexia nervosa in females. Female rats in proestrus showed higher basal plasma ACTH and CRF mRNA expression levels in the PVN and CeA than males. Females more rapidly showed higher plasma ACTH and corticosterone levels and a higher CRF mRNA expression level in the PVN in response to FS than males. Although females in both proestrus and diestrus showed significant increases in plasma ACTH and corticosterone and CRF mRNA expression in the PVN in response to PS, no significant responses of the HPA axis to PS were found in males. FS significantly increased CRF mRNA expression in the CeA in both females and males, with significantly higher peaks in females in proestrus than in males, while PS significantly increased CRF mRNA expression in the CeA only in males. These results suggest that gender affects differentially the function of the stress-related regions such as the PVN and CeA. The finding that CRF gene expression in the PVN responds to PS only in females may be a clue to elucidation of the neurobiological mechanism underlying the gender-differential prevalence of anorexia nervosa.

DOI： 10.1016/j.psyneuen.2008.09.003

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Urocortin 2 (Ucn 2) and Ucn 3 are new members of the corticotropin-releasing factor (CRF) family and bind selectively to the CRF type 2 receptor (CRF2). The effects of these peptides on behavioral changes induced by CRF were examined in rats. In a familiar environment, intracerebroventricular injection of Ucn 2 attenuated the stimulatory effect of CRF on motor activity, although it alone produced no effect. Ucn 3 suppressed motor activity and attenuated the stimulatory effect of CRF. In an open field, CRF decreased locomotion and rearing but increased grooming behavior. Ucn 2 attenuated the inhibition of locomotor activity induced by CRF without affecting other activities, such as rearing or grooming behavior. Ucn 3 had no effect on the behavioral changes induced by CRF, although it alone decreased locomotion and rearing in a manner similar to CRF. Ucn 2 was thus found to have an antagonistic effect on bi-directional motor activation induced by CRF, while Ucn 3 had a suppressive effect on motor activity. Both Ucn 2 and Ucn 3 suppressed food intake in freely-fed rats, but not immediately after injection. These results suggest that the CRF2 receptor is involved in motor suppressive effects as well as anxiolytic and anorectic effects of Ucn 2 and Ucn 3.

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

RATIONALE: Stress-induced inhibition of food intake is reportedly blocked by a selective corticotropin-releasing factor (CRF) type 1 receptor (CRF1) antagonist, suggesting the involvement of CRF1 in the inhibitory mechanism. CRF1 and CRF2 are considered to function in the inhibition of food intake by CRF-related peptides with different time courses. OBJECTIVES: This study was designed to clarify whether CRF2 is also involved in stress-induced inhibition of food intake and to examine the relation of CRF1to CRF2 in the inhibitory mechanism. METHODS: Antisauvagine-30 (AS-30), a selective CRF2 antagonist, and/or CRA1000, a selective CRF1 antagonist, were pre-administered intracerebroventricularly and intraperitoneally, respectively, to male Wistar rats deprived of food for 24 h before the animals were exposed to a 1-h period of stressors and food intake in 1 h after stress exposure was examined. The effect of both antagonists on locomotor activity was also examined. RESULTS: Pre-administration of 5-30 microg of AS-30 attenuated inhibition of food intake induced by restraint, electric footshock or emotional stress using a communication box. CRA1000 also attenuated the restraint-induced inhibition of food intake at doses of 5 and 10 mg/kg body weight. The reversal of restraint-induced inhibition of food intake by co-administration of AS-30 and CRA1000 was not larger than that by AS-30 or CRA1000 alone. Both antagonists did not affect locomotor activity. CONCLUSIONS: These results suggest that not only CRF1, but also CRF2, are involved in stress-induced inhibition of food intake, and that both subtypes of CRF receptor function probably in series in 1 h after stress exposure.

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

In adipocytes, peroxisome proliferator-activated receptor (PPAR)-gamma activates adipocyte differentiation and glucocorticoid (GC) stimulates the expression of PPAR-gamma mRNA. The local tissue concentrations of GC, in turn, are modulated by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). To clarify the change of energy metabolism in condition of reduced energy intake, we investigated whether food restriction alters the adipocyte size and levels of PPAR-gamma, GC receptor (GR), and 11beta-HSD1 mRNA expression in the white adipose tissues of normal rats. Male Wistar rats weighing 340 g were housed under free feeding or 20% reduction of food intake for 2 or 14 days. We found that 2-day food restriction did not cause any change in the mean size or number of adipocytes in the omentum, while 14-day food restriction decreased the size and increased the number of adipocytes. In addition, the levels of PPAR-gamma2, GR, and 11beta-HSD1 mRNA expression in the omentum were lower in the food-restricted rats after 2 days, while they did not differ after 14 days. Also, after both 2 and 14 days, plasma concentrations of free fatty acid (FFA) were higher in the food-restricted rats than in control rats. Finally, plasma concentrations of adrenocorticotropin (ACTH) and corticosterone were the same in the both groups after 2 days, although they were higher in the food-restricted rats after 14 days. These results suggest that adipocyte differentiation in the omentum of food-restricted rats is attenuated after 2 days but recovers after 14 days, resulting in an increase in the number of small adipocytes. It is also likely that lipolysis induced during the 14-day period of food restriction decreased the size of adipocytes. Further, food restriction may affect the efficiency of local GC effects by altering GR and 11beta-HSD1 mRNA expression. Also, higher levels of plasma GC and recovery of GR and 11beta-HSD1 mRNA expression may contribute to the recovery of the levels of PPAR-gamma2 mRNA expression in the omentum and result in the recovery of adipocyte differentiation.

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掲載種別：研究論文（学術雑誌）  

Several kinds of stress such as psychological stress, restraint, and foot shock inhibit feeding behavior through corticotropin-releasing factor (CRF). In contrast, a mild tail pinch increases food intake in rats. Although dopamine and opioid are thought to be involved in tail-pinch-induced food intake, it is unknown whether CRF participates in this phenomenon. Therefore, we attempted to clarify this issue using rats. A 30-s tail pinch increased food intake in 30 min after the tail pinch, and this increase was blocked by intraperitoneal injection of CRF receptor type 1 selective antagonist. CRF increased food intake in 30 min after intracerebroventricular injection at a dose of 2 or 10 ng, and this increase was also blocked by CRF receptor type 1 antagonist. Tail-pinch- or CRF-induced food intake was blocked by naloxone, pimozide, and spiperone. These results suggest that CRF, through CRF receptor type 1 as well as opioid and dopaminergic systems, are involved in the mechanism of tail-pinch-induced food intake. The results also suggest that brain CRF has dual effects on food intake, hyperphagia and anorexia, in a stress-dependent manner. © 2003 IBRO. Published by Elsevier Science Ltd. All rights reserved.

DOI： 10.1016/S0306-4522(02)00712-1

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Corticotropin-releasing factor (CRF) is involved in the regulation of stress responses. The actions of CRF in the brain are mediated through two distinct CRF receptor subtypes, CRF(1) and CRF(2) receptors. In the present study, we examined the effects in rat of chronic administration of a nonpeptidic CRF(1) receptor-selective antagonist, CRA1000, 2-[N-(2-methylthio-4-isopropylphenyl)-N-ethylamino]-4-[4-(3-fluorophenyl)-1,2,3,6-tetrahydropyridin-1-yl]-6-methylpyrimidine), on locomotor activity, feeding behavior and the hypothalamic-pituitary-adrenal axis. Chronic CRA1000 treatment significantly decreased locomotor activity in the dark phase of the diurnal cycle. However, chronic CRA1000 treatment showed no effect on food and water intake, or on body weight. After a 10-day period of CRA1000 treatment, plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone in basal conditions and under immobilization stress were no different from those in rats treated with vehicle. However, CRA1000 administered 2 h before immobilization stress significantly reduced ACTH and corticosterone responses to stress with no effect on basal ACTH and corticosterone concentrations. These results suggest that CRF(1) receptors are involved in the regulation of locomotor activity during the dark period, but are not involved in the regulation of feeding behavior under non-stressful conditions. Furthermore, the results suggest that a 10-day treatment with CRA1000 does not affect hypothalamic-pituitary-adrenal axis activity either under basal conditions or after acute stress.

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Growth hormone secretagogues (GHSs) stimulate GH secretion and food intake. GHS receptor (GHS-R) mRNA has been identified mainly in the arcuate nucleus (Arc) and ventromedial nucleus of the hypothalamus and in the pituitary. Ghrelin, an endogenous ligand for GHS-R, has recently been purified from rat stomach. Although ghrelin is also expressed in the hypothalamus, the physiological significance of the ghrelin/GHS-R system is still unknown. We have created transgenic (Tg) rats expressing an antisense GHS-R mRNA under the control of the promoter for tyrosine hydroxylase (TH), thus selectively attenuating GHS-R protein expression in the Arc. Tg rats had lower body weight and less adipose tissue than did control rats. Daily food intake was reduced, and the stimulatory effect of GHS treatment on feeding was abolished in Tg rats. GH secretion and plasma insulin-like growth factor-I levels were reduced in female Tg rats. These results suggest that GHS-R in the Arc is involved in the regulation of GH secretion, food intake, and adiposity.

DOI： 10.1172/JCI13300

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掲載種別：研究論文（学術雑誌）   出版者・発行元：American Physiological Society  

In the epileptic hippocampus, newly sprouted mossy fibers are considered to form recurrent excitatory connections to granule cells in the dentate gyrus and thereby increase seizure susceptibility. To study the effects of mossy fiber sprouting on neural activity in individual lamellae of the dentate gyrus, we used high-speed optical recording to record signals from voltage-sensitive dye in hippocampal slices prepared from kainate-treated epileptic rats (KA rats). In 14 of 24 slices from KA rats, hilar stimulation evoked a large depolarization in almost the entire molecular layer in which granule cell apical dendrites are located. The signals were identified as postsynaptic responses because of their dependence on extracellular Ca²⁺. The depolarization amplitude was largest in the inner molecular layer (the target area of sprouted mossy fibers) and declined with increasing distance from the granule cell layer. In the inner molecular layer, a good correlation was obtained between depolarization size and the density of mossy fiber terminals detected by Timm staining methods. Blockade of GABAergic inhibition by bicuculline enlarged the depolarization in granule cell dendrites. Our data indicate that mossy fiber sprouting results in a large and prolonged synaptic depolarization in an extensive dendritic area and that the enhanced GABAergic inhibition partly masks the synaptic depolarization. However, despite the large dendritic excitation induced by the sprouted mossy fibers, seizurelike activity of granule cells was never observed, even when GABAergic inhibition was blocked. Therefore, mossy fiber sprouting may not play a critical role in epileptogenesis.

DOI： 10.1152/jn.2000.83.4.2421

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/s0006-8993(99)02378-1

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/s0304-3940(98)00719-8

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記述言語：日本語   出版者・発行元：日本医科大学医学会  

It is reported that chronic electrical stimulation of perforant path (PP) produces mossy fiber sprouting in dentate granule cells and as a result new reccurent excitatory circuits are formed. It has been assumed that the circuits are responsible for the well-known lowering in the threshold required to generate seizure discharges by the electrical stimulation. The assumption was tested in the present investigation. Current source density analysis of the field potential in the dentate gyrus was carried out in control (n=8) and kindled (n=10) rats under pentobarbital anesthesia during seizure discharges. The field potential was produced by stimulating the PP and recorded simultaneously from 10 sites which were 50 μm apart from each other. The field potential consisted of a monosynaptic excitatory postsynaptic field current (EPSC) in the middle molecular layer followed by a population spike current (PSC). In the kindled rats, following the EPSC and PSC, a late sink appeared in the supragranular layer (SGL). The amplitude of the SGL late-sink showed a positive correlation with the density of Timm granules (r=0.76). The latency difference between the onset of PSC and that of the SGL late-sink ranged from 0.5 to 1.5 ms. This suggested the possibility that the SGL late-sink is produced via the recurrent excitatory circuit newly formed by mossy fiber sprouting. The SGL late-sink, however, evoked no further firing in dentate granule cells. During 5 Hz PP stimulation for 10 s, the amplitude of SGL late-sink increased gradually at first, but later it decreased gradually and disappeared before seizure discharges produced. Accordingly, there was no evidence suggesting that the new recurrent excitatory circuit played any role in producing seizure discharges. During seizure discharges, the EPSC resembling the SGL late-sink appeared spontaneously only in the SGL and seemed to initiate repetitive synchronized-firing of granule cells in one of four kindled rats. The number of burst discharges and the duration of seizure discharges with the late sink, however, were not significantly different from those of seizure discharges without such a late skin. These results suggest that the newly formed recurrent circuit plays no essential role in decreasing the threshold required to generate seizure discharges or in developing them. (J Nippon Med Sch 1997 ; 64 : 154-162)

DOI： 10.1272/jnms1923.64.154

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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：The Japanese Pharmacological Society  

A novel serotonin reuptake inhibitor, (-)trans 4-(4-fluorophenyl)-3-(4-methoxyphenoxy-methyl)piperidine hydrochloride (FG-7080), was investigated for its effects on scopolamine-induced impairments in memory tasks of rats. In the radial-arm maze task, FG-7080 (3 mg/kg, p.o.) improved the impaired performance. FG-7080 (1 mg/kg, p.o.) administered before the acquisition trial reduced the acquisition deficits in the passive avoidance task. Thus, the compound showed improving effects in the appetitive and aversive memory tasks. These findings suggest that FG-7080 may ameliorate the cognitive impairments caused by the cholinergic dysfunction.

DOI： 10.1254/jjp.62.203

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総ページ数：xvi, 494 p.   記述言語：英語  

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記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

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記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

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記述言語：日本語  

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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：(一社)日本内分泌学会  

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記述言語：日本語  

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出版者・発行元：日本生理学会  

Interleukin-18 (IL-18), known as interferon-&gamma; inducing-factor, exerts pleiotropic roles as a potent pro-inflammatory cytokine. In addition to immune cells, it has been demonstrated in rat adrenal cortex, posterior pituitary gland, and medial habenular nucleus and bovine somatotrophs. Although IL-18 has been demonstrated to increase in obesity, diabetus mellitus, ischemic heart diseases and autoimmune diseases, the mechanism by which the induction of IL-18 occurs in vivo remains to be elucidated. To clarify the secretary mechanism of IL-18 into circulation, the present study investigated IL-18 levels in response to immobilization, cold, sleep deprivation, and lipopolysaccharide (LPS). In addition, to speculate the source of IL-18, adrenectomy was conducted. The mean IL-18 level under control condition was 189 &plusmn; 1.0 pg/ml. In immobilization stress for 1 h and 2 h, its levels significantly increased to 222.3 &plusmn; 2.2 pg/ml (p<0.05) and 220.7 &plusmn; 0.8 pg/ml (p<0.001), respectively. Of important notice, its levels further went up in 2 h after the 2-h immobilization stress (320.5 &plusmn; 7.7 pg/ml, p<0.05). A significant increase was also observed in cold stress (226 &plusmn; 2.9 pg/ml, p<0.05), while no significant change occurred in sleep deprivation. In adrenectomized mice IL-18 levels significantly increased in response to LPS, but not to stressors. LPS significantly up-regulated IL-18 mRNA expression in the spleen, but not in the adrenal gland. The present results show the tissue-specific induction of IL-18 gene expression, and suggest that adrenal cortex may be the main source of IL-18 which increases in blood during stress. [Jpn J Physiol 54 Suppl:S219 (2004)]

DOI： 10.14849/psjproc.2004.0_S219_4

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記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

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記述言語：日本語   出版者・発行元：間脳・下垂体・副腎系研究会  

anti-sauvagine-30(AS-30)を脳室内投与後に拘束,フットショック,心理ストレスを負荷し,ストレス負荷後1時間の摂食量を測定して,各々のストレスによる摂食抑制機序へのCRFR2の関与の有無を検討した.又,CRA1000及びAS-30の両投与の拘束による摂食抑制への影響を検討した.拘束,フットショック,心理ストレスなどのストレスによる摂食抑制をCRFR2選択的拮抗薬であるAS-30が阻止し,摂食量を回復させ,CRFR2がストレス時の摂食抑制機序に関与していることを示唆された.よって,拘束,フットショック,心理ストレスによる摂食抑制機序にはCRFR1のみならずCRFR2も関与していることが示唆された

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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：(一社)日本内分泌学会  

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記述言語：日本語   出版者・発行元：間脳・下垂体・副腎系研究会  

副腎皮質刺激ホルモン放出因子(CRF)ペプチドファミリーのウロコルチン(Ucn) IIおよびUcn III におけるUcn IIの免疫組織化学検索と摂食行動,運動活動量に与える両ペプチドの作用をマウスとラットを用いて検討した.免疫組織化学方法ではマウス・ラット共に視床下部室傍核に陽性細胞が多く認められ,視床下部弓状核において少量の陽性細胞と多数の陽性線維が認められた.Ucn IIは投与後6時間より9時間で,Ucn IIIは投与後4時間より8時間で摂食量がvihicleを投与したラットに比べ有意に減少した.ラットにおける両ペプチドの投与による摂食量の減少は見られなかった.ホームゲージにおける運動活動量は,CRF投与後4時間にわたり活動量の上昇が見られ,Ucn IIIのみを投与したラットでは活動量を低下させることが示された.また,CRFによる行動変化に対してUcn IIが拮抗して作用することが示唆された

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記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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掲載種別：記事・総説・解説・論説等（国際会議プロシーディングズ）  

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記述言語：日本語   出版者・発行元：日本動物心理学会  

CiNii Books

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記述言語：日本語   出版者・発行元：日本てんかん学会  

CiNii Books

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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：筑波大学心理学系  

CiNii Books

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記述言語：日本語   出版者・発行元：日本動物心理学会  

CiNii Books

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記述言語：日本語   出版者・発行元：日本動物心理学会  

CiNii Books

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：英語  

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記述言語：日本語  

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記述言語：英語  

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記述言語：日本語  

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記述言語：日本語  

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会議種別：ポスター発表  

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記述言語：日本語  

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記述言語：日本語  

開催地：浜松市  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

開催地：東京  

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記述言語：英語  

開催地：Toronto, Canada  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

開催地：前橋  

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記述言語：日本語  

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記述言語：英語  

開催地：Washington, DC, USA  

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記述言語：日本語  

開催地：前橋  

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記述言語：日本語  

開催地：京都  

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記述言語：日本語  

開催地：北九州  

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記述言語：英語  

開催地：浜松  

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記述言語：日本語  

開催地：東京  

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記述言語：英語  

開催地：金沢  

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記述言語：日本語  

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記述言語：日本語  

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会議種別：ポスター発表  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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記述言語：日本語  

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