Objective To explore whether heat acclimation can protect the structure and function of mitochondrion of cerebral cortex and myocardium in rats with moderate and high intensity exercise in hygrothermal environment,and to explore its protective mechanism.Methods Forty SD rats underwent swimming experiment bearing weight and 8 rats were eliminated due to too short-swim or long-swim time.The rest 32 rats were randomly divided into four groups (n=8):room-temperature activity (RA) group,room-temperature exercise (RE) group,high-temperature activity (HA)group and high-temperature exercise (HE) group.Rats in RA and HA groups were placed at room temperature ([24± 1] ℃) and high temperature ([32±1] ℃) to have a free activity for 2 h/d.Rats in RE and HE groups were placed at room temperature ([24±1] ℃) and high temperature ([32± 1] ℃) to have a free activity for 1 h/d and then were allowed to run at a constant speed on the animal treadmill for 1 h/d (slope:0°,speed:14 m/min).After 14 days the heat acclimation rat models were created.Rats in all groups underwent moderate and high intensity exercise in hygrothermal environment for 30 min on the 3rd day.The body weight loss rate and rectal temperatures of rats were measured before and after high and medium intensity exercise in hygrothermal environment.The contents of plasma norepinephrine (NE),arginine vasopressin (AVP) and cortisol (Cort) in rats were detected by radioimmunoassay.The ultrastructure of the mitochondria of cerebral cortex and myocardium was observed by transmission electron microscopy.The contents of ATP synthase and reactive oxygen species (ROS) were detected by ELISA method and the total antioxidative capacity was measured by ABTS method.Results The rectal temperatures before and after stimulation and the ascending range of rectal temperatures of rats in HE group were significantly lower than those in the RA,RE and HA groups (P＜ 0.05,P＜0.01).After stimulation with moderate and high intensity exercise in hygrothermal environment,the body weight loss rate of rats in HE group was significantly higher than that in RA group (P＜0.01),the contents of plasma Cort and ROS of rats in HE group were significantly lower than those in the RA,RE and HA groups (P＜0.05,P＜0.01),the content of ATP synthase in mitochondrion and total antioxidative capacity in tissue from cerebral cortex and myocardium of rats in HE group were significantly higher than those in the RA,RE and HA groups (P ＜ 0.01),and the mitochondrion and synaptic structures in the cerebral cortex and the structures of myocardium,Z line and transverse tubule in the myocardium in HE group were superior to those in the RA,RE and HA groups.Conclusion Heat acclimation can enchance the oxidative and respiratory function of mitochondria and reduce the level of cell oxidative stress and the content of plasma Cort,so as to protect the mitochondrial structure of cerebral cortical neurons and cardiomyocytes in rats with moderate and high intensity exercise in hygrothermal environment.

Background: Hippocampal functions are sensitive to sleep deficiency. Dopamine D1 receptor (D1R) in hippocampus can regulate the expression of cAMP response element binding protein (CREB) through PICA, MAPK and phosphoinositide pathway, but which pathway plays the major role in hippocampus during Chronic sleep deprivation (CSD) is unclear.Methods: The CSD model was created, SKF rats were administered the D1R agonist (SKF38363), and hippocampus from each animal was dissected for following molecular detection. The gene and protein levels of CREB and key molecules in D1R pathways were measured by real-time PCR and western blotting, respectively.Results: Both the gene and protein expression of CREB in hippocampus decreased by CSD and improved significantly by SKF38393 (p <0.05). Both the gene and protein expression of PICA in hippocampus decreased by CSD and improved significantly by SKF38393 (p <0.05). SKF38393 just significantly improved the gene level of CaMK IV and the protein level of p-CaMIC IV (p <0.05) in CSD rats, but it cannot improve the protein expression of ERK1/2 and p-ERK1/2.Discussion: CSD significantly decreased the expression of CREB in hippocampus. As the key molecules, PICA and CaMK IV play an important role during the improvement of hippocampus by the activation of D1R, and this process might be improved during CSD through the PICA and phosphoinositide pathway. (C) 2017 Elsevier B.V. All rights reserved.

通过调查明确热带医学专业本科应突出培养学生哪些方面的知识、能力和技能;并运用自制的能力培养需求量表调查了军医大学热带医学与公共卫生学系教师23名、部队军医22名、部队卫生领导20名.结果 表明,职业素质、临床技能、沟通技能和预防医学专业技能等解决实际问题的能力与技能受到调查对象的重视.提示在热带医学本科生培养过程中,应将目标定位在培养学生解决实际问题的能力上,课程设置应突出热带医学的专业特点和实践能力的培养.

Objective To investigate the effects of different thermal conditions on the heat acclimatization and physical ability of rats in hot and humid environment .Methods Sixty-four male SD rats were randomly divided into 8 groups:the normal temperature and humidity rest group ( or the NTHR group );the normal temperature and humidity exercise group ( or the NTHE group );the normal temperature and high humidity rest group ( or the NTHHR group ); the normal temperature and high humidity exercise group ( or the NTHHE group);the high temperature and normal humidity rest group (or the HTNHR group); the high temperature and normal hu-midity exercise group ( or the NTNHE group );the high temperature and humidity rest group ( or the HTHR group ) and the high tem-perature and humidity exercise group (or the HTHE group), each consisting of 8 animals.Every day, the rats of the rest groups were left there at rest in the corresponding environment , while the rats of the exercise groups were first left there at rest for an hour , then had exercise at a load of 14 m/min for an hour for a succession of 14 days.Every day, all the rats were weighed both before and after exper-iment, the rate of weight loss was calculated and rectal temperature was taken the moment after the experiment was terminated .At day 16, all the rats had exercise at high temperature (36℃) and high humidity (85%) environment at a load of 28 m/min for 30 minutes. The number of the exhausted rats and exhaust time were recorded during exercise , and at the same time , the levels of rectal temperature were taken the moment after exhaust and when the exercise was terminated .At day 17, the number of rats that died of exhaust was cal-culated and recorded .Results In the course of heat acclimatization , the rate of weight loss at day 4 for all the animals groups except the groups at high temperature/rest began to decrease considerably (P<0.05).The rectal temperature of the animals in the high tem-perature/rest group and the high temperature/exercise group began to drop significantly at day 4(P<0.05).The rectal temperature and weight loss rate of the rats in the 4 exercise groups were significantly higher than those of the 4 rest groups (P<0.05).Furthermore, the rectal temperature of the HTHE group was significantly higher than that of the HTNHE group (P<0.05), however, there was no significant difference in the rate of weight loss , when comparisons were made between the two groups (P>0.05).Following physical exercise at high temperature and high humidity , the rectal temperature and the number of the rats with exhaust in the midst of the exer-cise and the number of deaths the next day in the HTNHE and HTHHE groups were significantly lower than those in the NTNHR and HTHHR groups (P<0.01).However, no significant differences could be seen between the HTNHE group and the HTHHE group (P>0.05).Conclusion Exercises at high temperature/high humidity and high temperature/normal humidity could achieve best heat accli-matization effect .From the standpoint of least effect on body temperature and weight loss , training at high temperature/normal humidity environment is a more appropriate heat acclimatization method .

生物恐怖事件医学救援物资装备保障,是有效组织实施防生救援的关键环节之一.本文结合实践经验,分析生物恐怖事件医学救援队伍物资装备保障的特点与难点,探讨救援队伍物资保障与个人装备保障的主要做法,并总结物资装备配备应注意的主要问题.

目的 探讨大鼠经热习服及后续热环境运动刺激后血浆中代谢产物的变化特征,筛选热习服特异性的指示标志物.方法 将16只SD大鼠随机分为热习服组和对照组(n=8),热习服组大鼠经每日2h热习服训练,对照组大鼠不做相应处理,连续14d,结束后次日采集两组大鼠眼眶血.休息4d后所有大鼠均经热环境运动刺激30 min,麻醉后取腹主动脉血并离心取血浆.使用Bruker 600 MHz核磁共振谱仪检测两组大鼠血浆中代谢产物的1 HNMR谱,分析热习服及热环境运动刺激后大鼠血浆代谢产物的变化.结果 与对照组相比,热习服组大鼠在热习服后血浆中不饱和脂肪酸、谷氨酸、脂质和二甲胺的含量升高,而葡萄糖、肌醇、牛磺酸、苏氨酸和三甲胺氧化物含量均下降(P＜0.05);而在热环境运动刺激后,热习服组大鼠血浆中三甲胺氧化物、谷氨酸和脂质的含量均下降(P＜0.05).结论 经热习服和热环境运动刺激后,大鼠血浆中代谢物质发生了明显变化.三甲胺氧化物有可能作为热习服的指示性标志物,为制定热习服客观评价体系提供有意义的线索.

Objective To study and analyze the features and pattern of the common diseases occurred among recruits of a certain naval unit during training,so as to provide reference for the prevention of diseases.Methods Medical data files in the medical corps were sorted out,and were then classified according to the types of diseases,and finally were analyzed statistically.Results During recruit training,through outpatient service,inpatient service and medical tours or calls,there were 362 cases of various diseases,accounting for 22.3％ of all the recruits engaged in the recruit training.The top three diseases were:infection of the upper respiratory tract,with 128 cases,accounting for 7.88％,soft tissue injury of extremities with 68 cases,accounting for 4.18％ and oral diseases with 22 cases,accounting for 1.35％.From the perspective of diseases incidence,the top 3 disease respectively accounted for 35.4％,18.8％ and 6.1％,with a total incidence of 60.3％ of all the diseases.Conclusions Closer attention to the weak links in disease prevention and better prevention and treatment measures against the common disease among the recruits were the surest guarantee for the reduction of incidence and improvement of training results.

运用自制的临床医学(热带医学专业方向)课程设置需求量表,在部队卫勤领导、部队军医、军医大学热带医学与公共卫生学系教师中进行调查.结果表明,野战外科学、野战内科学、热带传染病学、热带军队流行病学等课程,以及突出实践能力培养的课程受到调查对象的重视,提示在热带医学专业方向培养过程中,课程体系设置要突出专业特点,要突出实用性,教学过程中要注重培养学生的实践能力.

CNS Neuroscience & TherapeuticsVolume 19, Issue 9 p. 730-733 Letter to the EditorOpen Access The Regulation of SKF38393 on the Dopamine and D1 Receptor Expression in Hippocampus during Chronic REM Sleep Restriction Xiao-Sa Wen, Xiao-Sa Wen Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, ChinaSearch for more papers by this authorXin-Min Chen, Xin-Min Chen Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, ChinaSearch for more papers by this authorFei Rong, Fei Rong Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, ChinaSearch for more papers by this authorTao Jing, Tao Jing Department of Biological Sciences, University of Alabama, Tuscaloosa, Alabama, USASearch for more papers by this authorSi Chen, Si Chen School of Kinesiology, Shanghai University of Sport, Shanghai, ChinaSearch for more papers by this authorWen-Ling Ma, Corresponding Author Wen-Ling Ma Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, China Correspondence Wen-Ling Ma, Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai 200433, China. Tel.: +86-139-1786-1579; Fax: +86-21-8187-1110; E-mail: wenlingma@163.comSearch for more papers by this author Xiao-Sa Wen, Xiao-Sa Wen Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, ChinaSearch for more papers by this authorXin-Min Chen, Xin-Min Chen Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, ChinaSearch for more papers by this authorFei Rong, Fei Rong Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, ChinaSearch for more papers by this authorTao Jing, Tao Jing Department of Biological Sciences, University of Alabama, Tuscaloosa, Alabama, USASearch for more papers by this authorSi Chen, Si Chen School of Kinesiology, Shanghai University of Sport, Shanghai, ChinaSearch for more papers by this authorWen-Ling Ma, Corresponding Author Wen-Ling Ma Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai, China Correspondence Wen-Ling Ma, Department of Environmental Hygiene, Faculty of Tropical Medicine and Public Health, Second Military Medical University, Shanghai 200433, China. Tel.: +86-139-1786-1579; Fax: +86-21-8187-1110; E-mail: wenlingma@163.comSearch for more papers by this author First published: 04 July 2013 https://doi.org/10.1111/cns.12140Citations: 7 The first two authors contribute equally to this work. AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat A large amount of data have demonstrated that sleep deprivation, including acute sleep deprivation (ASD) and chronic sleep restriction (CSR), can negatively affect spatial learning and working memory through disrupting hippocampal function 1, 2. The hippocampus, which plays an important role in cognition and emotional regulation, receives strong dopaminergic input from midbrain dopaminergic neurons. Dopamine (DA) D1 receptor (D1R) is critical for long-term potentiation (LTP), spatial learning, and related signaling in the hippocampus 3, 4. SKF38393, as a selective D1R agonist, can significantly increase waking and reduce rapid eye movement (REM) sleep 5. Recent studies have indicated that there are similar ASD and CSR symptoms in humans and animals. Compared with ASD, the effect of CSR on neurobiological mechanisms of the hippocampus is still not fully understood. It is still unclear that by what mechanism CSR affects the neuronal ultrastructure and dopaminergic system in the hippocampus. Therefore, using a protocol of intermittent sleep deprivation with the flower pot technique 6, we produced a model of chronic REM sleep restriction in rats to study: (1) whether CSR could change hippocampal ultrastructure, DA concentration, and D1R expression as it was changing the behavior of rats, and (2) how did SKF38393 improve these conditions during the late phase of CSR. A total of 90 male Sprague-Dawley rats, weighing 250 ± 10 g, were used in the present experiments. The animals were obtained from the laboratory animal center of the Second Military Medical University (SMMU), and all the animal protocols were approved by the Ethical Committee of the Second Military Medical University (SMMU), Shanghai, China. After 3 days of training, 15 rats were removed either because the escape latency was more than 90 seconds at each trail or the rats failed to stand on platforms constantly. The remaining 75 rats were randomly divided into three groups (n = 25 in each): treatment control (TC), chronic sleep restriction (CSR), and SKF38393 administration (SKF). The CSR model was created using modified multiple platform method (MMPM) 6. Animals were housed in a room with a 12-h/12-h light/dark cycle (lights on at 8:00 am) and at temperature of 22 ± 1°C. Standard laboratory chow and water were provided ad libitum. Rats in CSR and SKF groups were kept on the platforms (in diameter 6.5 cm) surrounded by water for 18 h (beginning at 4:00 pm) and then allowed to sleep for 6 h in their individual home cages (10:00 am–4:00 pm) per day. Rats in TC group were placed on the wire entanglement in box to allow moving and sleeping freely in a similar water environment. After 14 days of CSR, rats in the SKF group were administered SKF38393 (1 mg/kg dissolution in 1 mL PBS, i.p.; Sigma, St. Louis, MO, USA) at 10:00–11:00 am for seven consecutive days, and SKF38393 was replaced by PBS, using as a solvent control in the TC and CSR groups. The animals were weighed before the procedure and on alternate days during the CSR, and Morris water maze was used to measure the ability of learning and memory. The animals were trained to find the hidden platform according to the spatial cues in the experimental room, and the escape latency was tracked by the video tracking system (Jiliang Limited Co., Shanghai, China). The performances in the Morris water maze were observed on the first 3 days of training and after 7, 14, and 21 days of CSR. On day 21 of CSR, both the open-field test and load swimming were performed. After 22 days of CSR, the rats were perfused with 4°C saline through the ascending aorta under chloral hydrate anesthesia (400 mg/Kg, i.p.). Then, hippocampi taken from 20 animals in each group were dissected under operating microscope. The samples were stored in −80°C for following experiments. The DA concentration and the D1R expression in the hippocampus were determined by high-performance liquid chromatography with electrochemical detection (ESA, Chelmsford, MA, USA), real-time PCR, and Western blot method. The last five rats in each group were fixed with 2.5% glutaraldehyde and 4% paraformaldehyde; the tissue samples were cut into ultrathin sections and then photographed under transmission electron microscope (H-7650; Hitachi, Tokyo, Japan). Within the randomly selective five frames for each group, the number of damaged and total mitochondria was counted, and then, the percentage of damage was calculated. The body weight was gradually increased in TC group during the CSR, and it began to obviously decrease in CSR and SKF groups on the third day of CSR (Figure 1A). After 21 days of CSR, the loading swimming time to exhaustion was significantly shortened in CSR and SKF groups compared with that in TC group (Figure 1B). There were no notable differences in the weight and stamina between CSR and SKF groups. After 21 days of CSR, although the escape latency was still prolonged and the quadrant dwell time was clearly reduced in the SKF group compared with those in the TC group, they were significantly improved compared with CSR group (Figure 1C,D). Furthermore, compared with CSR group, there was an obvious increase in the total distance and activity times in SKF groups, but compared with TC group, the locomotor activity was still significantly decreased in SKF group (Figure 1E,F). Figure 1Open in figure viewerPowerPoint Effect of chronic sleep restriction (CSR) and SKF38393 on the behavioral changes. (A) Weight in CSR and SKF groups did not increase normally during CSR. (B) Load swimming time to exhaustion in CSR and SKF groups showed significant reduction. (C) Both CSR and SKF rats spent significantly more time than TC rats to find the hidden platform, and SKF rats displayed significantly shorter escape latency than CSR rats on 21st day of CSR. (D) Both CSR and SKF rats spent notable less time in target quadrants during CSR, and SKF rats displayed notable longer quadrant dwell time than CSR rats on 21st day of CSR. (E, F) The total distance and activity times were significantly decreased in CSR and SKF groups compared with TC group, while the locomotor behaviors in SKF group displayed obviously better than CSR group. TC, treatment control; CSR, chronic sleep restriction. SKF, SKF38393 administration. **, P < 0.01 CSR group versus TC group; ##, P < 0.01 SKF group versus TC group; ΔΔ, P < 0.01 SKF group versus CSR group; Δ, P < 0.05 SKF group versus CSR group; n = 25 per group, results are expressed as ± SD. Under the transmission electron microscope, the damages of the mitochondria were identified by the fragmentation of membrane and fuzzy of cristae. Only 11.9% (10/84) abnormal mitochondria were observed in TC group, while in CSR group, 41.0% (34/83) mitochondria were damaged, and in SKF group, the percentage of damage is 24.3% (9/37). Furthermore, the general ultrastructure in TC group looked normal, while in CSR group, the degeneration of postsynaptic dense zone, fuzzy of synaptic vesicles, and abnormal dense bodies in the cytoplasm were found. However, the damage of ultrastructure in SKF group was notably improved, showing that the postsynaptic dense zone became thicker and clearer, and the number of synaptic vesicles was increased (Figure 2A). As shown in Figure 2B, CSR caused a significant decrease in the concentration of hippocampal DA, and treatment with SKF38393 led to a clear increase in this in SKF group. In addition, after CSR, the expression of D1R at transcriptional and translational level was significantly reduced in CSR group while increased in SKF group (Figure 2C–E). Figure 2Open in figure viewerPowerPoint Results of morphological and biochemical determination. (A) Electron micrographs of hippocampus in each group after chronic sleep restriction (CSR): compared with TC group (A1), CSR group (A2) showed that the membrane structure and cristae of mitochondria (arrowheads) were damaged or disappeared; the postsynaptic density (thick arrows) became disrupted and thinner, the synaptic vesicles (thin arrows) became fuzzy and minor, and the neuronal ultrastructure in SKF group (A3) returned mostly to normal (scale bar = 1 um, n = 5). (B) CSR significantly decreased the DA content in hippocampus, and SKF38393 reversed this reduction (n = 8). (C) CSR caused the significant decrease in D1R mRNA in hippocampus and SKF38393 obviously increased that of SKF group, even compared with TC group (n = 6). (D, E) CSR significantly decreased the level of D1R in hippocampus, and SKF38393 reversed this reduction (n = 6). TC: treatment control; CSR: chronic sleep restriction. SKF, SKF38393 administration. **, P < 0.01 CSR group versus TC group; ##, P < 0.01 SKF group versus TC group; ΔΔ, P < 0.01 SKF group versus CSR group, and results are expressed as ± SD. Our findings demonstrate that although SKF38393 administration during the late phase of CSR cannot change the loss of weight and stamina, it may partially improve the deficiency of spatial learning and memory induced by CSR and enhance the explorative activity. At the same time, it can also protect the hippocampal ultrastructure and the function of dopaminergic system in hippocampus during the late phase of CSR. CSR cannot only decrease hippocampal volume but also induce apoptosis and calcium overload in the hippocampus of rats 7, 8. The present study further demonstrates that CSR can lead to the destruction of the hippocampal neuronal ultrastructure, including the swelling of mitochondria and the damage of synaptic structure, whereas the changes in hippocampal ultrastructure are significantly improved by SKF38393. The mitochondria are the center of energy production in cells and related to apoptosis; thus, improvement in its structure might enhance the neural energy supply and then ameliorate metabolic activity and function of neurons. Changes in hippocampal neuron morphology are consistent with the changes in the learning and memory ability of CSR and SKF39383-administered rats. Previous study indicated that by inhibiting the cAMP-PKA-CREB signaling pathway, ASD could cause plasticity change in hippocampal synaptic structure and functions, including the LTP inhibition and membrane excitability reduction 9. The increase in hippocampal activity would improve the function of learning and memory during CSR, but this mechanism has remained unclear. In this article, we found that SKF38393 could enhance DA concentration and D1R expression in hippocampus during CSR. The D1R, as a G-protein-couple receptor for activation, can modulate the transcriptional level and protein expression by cAMP-PKA-CREB signaling pathway 9. Besides, it can also interact with glutamate NMDA receptor to enhance LTP and neural excitability through this pathway 10. Therefore, stimulation of D1R may improve the dysfunction of hippocampus induced by CSR. Because the hippocampus plays a critical role in the learning and memory ability, the activation of hippocampal D1R might become an important way to improve the cognitive dysfunction caused by CSR. However, in the present study, the D1R agonist injected into the abdominal cavity may affect D1R all over the central nervous system. If the D1R agonist could be injected directly into hippocampus in future study, it would conduce to further demonstrating this mechanism. Acknowledgements This work was supported by National Nature Science Foundation of China (81172638). Conflict of Interest The authors declare no conflict of interests. References 1Orzel-Gryglewska J. Consequences of sleep deprivation. Int J Occup Med Environ Health 2010; 23: 95– 114. CrossrefPubMedWeb of Science®Google Scholar 2Armani F, Andersen ML, Andreatini R, et al. Successful combined therapy with tamoxifen and lithium in a paradoxical sleep deprivation-induced mania model. CNS Neurosci Ther 2012; 18: 119– 125. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar 3Xing B, Kong B, Meng X, et al. Dopamine D1 but not D3 receptor is critical for spatial learning and related signaling in the hippocampus. Neuroscience 2010; 169: 1511– 1519. CrossrefCASPubMedWeb of Science®Google Scholar 4Granado N, Ortiz O, Suárez LM, et al. D1 but not D5 dopamine receptors are critical for LTP, spatial learning, and LTP-induced arc and zif268 expression in the hippocampus. Cereb Cortex 2008; 18: 1– 12. CrossrefPubMedWeb of Science®Google Scholar 5Monti JM, Monti D. The involvement of dopamine in the modulation of sleep and waking. Sleep Med Rev 2007; 11: 113– 133. CrossrefPubMedWeb of Science®Google Scholar 6Machado RB, Suchecki D, Tufik S. Sleep homeostasis in rats assessed by a long-term intermittent paradoxical sleep deprivation protocol. Behav Brain Res 2005; 160: 356– 364. CrossrefPubMedWeb of Science®Google Scholar 7Novati A, Hulshof HJ, Koolhaas JM, et al.Chronic sleep restriction causes a decrease in hippocampal volume in adolescent rats, which is not explained by changes in glucocorticoid levels or neurogenesis. Neuroscience 2011; 190: 145– 155. CrossrefCASPubMedWeb of Science®Google Scholar 8Souza LD, Smaili SS, Ureshino RP, et al. Effect of chronic sleep restriction and aging on calcium signaling and apoptosis in the hippocampus of young and aged animals. Prog Neuropsychopharmacol Biol Psychiatry 2012; 39: 23– 30. CrossrefCASPubMedWeb of Science®Google Scholar 9Vecsey CG, Baillie GS, Jaganath D, et al. Sleep deprivation impairs cAMP signalling in the hippocampus. Nature 2009; 461: 1122– 1125. CrossrefCASPubMedWeb of Science®Google Scholar 10Wang M, Wong AH, Liu F. Interactions between NMDA and dopamine receptors: a potential therapeutic target. Brain Res 2012; 1476: 154– 163. CrossrefCASPubMedWeb of Science®Google Scholar Citing Literature Volume19, Issue9September 2013Pages 730-733 FiguresReferencesRelatedInformation

Repeated exposure to a provocative motion stimulus leads to motion sickness habituation indicative of the existence of central processes to counteract the disturbing properties of the imposed motion. In the present study, we attempt to investigate whether NMDA and GABAA receptors in rat caudal vestibular nucleus neurons are involved in motion sickness habituation induced by repeated Ferris-wheel like rotation in daily session (2 h/d). We showed that defecation response increased and spontaneous locomotion decreased within 4 sessions (sickness phase). They recovered back to the control level after 7 sessions (habituation phase). Western blot analysis found that NMDA receptor signal molecules: calmodulin protein kinase II and cAMP response element-binding protein (CREB) were both activated during sickness phase, while a prolonged CREB activation was also observed during habituation phase. Real-time quantitative PCR revealed an increase in c-fos and a decrease in Arc mRNA level during sickness phase. We also found an increase in GABAA receptor α1 subunit (GABAA α1) protein level in this stage. These results suggested that altered NMDA receptor signaling and GABAA receptor expression level in caudal vestibular nucleus were associated with motion sickness habituation. Furthermore, immunofluorescence and confocal laser scanning microscopy showed that the number of GABAA α1 immunolabeled neurons in caudal vestibular nucleus increased while the number of GABAA α1/Arc double labeled neurons and the average amount of Arc particle in soma of these neurons decreased during sickness phase. It suggested that GABAA receptor level might be negatively regulated by Arc protein in caudal vestibular nucleus neurons.

Objective To study the seasickness assessment scale applicable to the Chinese population.Methods The questionnaire containing signs and symptoms from the Graybiel,the Wiker and other scales was used to investigate the signs and symptoms of 505 ordinary Chinese with seasickness.Results(1)Besides vomiting,retching,and the"five cardinal symptoms",other symptoms more frequently reported among ordinary Chinese population were dizziness,fatigue,yawning,anorexia,warmth,headache,etc.(2)Ordinary subjects with little medical background had difficulty in comprehension of symptoms described in the Wiker questionnaire.(3)In some cases,certain subjects either minimized or exaggerated symptoms of seasickness.(4)In the dim light of ship compartments,certain symptoms such as pallor,sweating,etc.could only be recognized through careful observation by the researchers,subjects or people around them.(5)In the light of the above problems,a modified seasickness assessment scale and seasickness score based on the Wiker scale was thus developed.Conclusions There were some limitations in the on-site assessment of seasickness severity for the ordinary Chinese population either with the Graybiel scale or the Wiker scale.The modified seasickness questionnaire and grading method were more simple and effective.

We investigated the temporal change of Fos protein expression in the caudal vestibular nucleus of rats exposed to daily 2-h Ferris-wheel like (FWL) rotation. Repeated rotation (2h daily for 14 consecutive days) caused an initial increase in defecation, followed by a gradual decline back to the baseline level after 8 rotation sessions. Unlike defecation, the Kaolin consumption of rats showed a bitonic function during the daily rotation sessions (2h daily for 33 consecutive days) and finally recovered to the baseline after about 31 sessions. Immunohistochemistry study revealed increased Fos immunolabeled (Fos-LI) neurons in the medial vestibular nucleus and spinal vestibular nucleus during the initial 7 rotation sessions, and it decreased to the baseline level after 10 rotation sessions. There was a strong linear relationship between the amount of Fos-LI neurons and rat defecation level throughout the whole rotation sessions. These results suggest that the change of neuronal plasticity in the caudal vestibular nucleus might contribute to attenuation of gastrointestinal symptoms during motion sickness habituation process.

目的 观察不同剂量支链氨基酸、酪氨酸以及二者复合配方对晕船模拟刺激后大鼠脑体疲劳恢复的影响.方法 大鼠分为空白对照组、晕船组和6个干预组(高支组、低支组、高酪组、低酪组、高复组、低复组),共8组,喂养10 d后,进行晕船刺激,通过旷场实验和Morris水迷宫观测大鼠晕船后的活动度和认知能力,通过负重游泳实验观测各组大鼠晕船后体能差别.结果 晕船大鼠负重游泳时间短于空白对照组(P＜0.01),而高支组、低支组、低复组的游泳时间显著长于晕船组和其他3个干预组(P＜0.05);低支组、高酪组、低酪组、高复组以及低复组旷场实验得分显著高于晕船组(P＜0.01),而和空白对照组之间差异无统计学意义;Morris水迷宫实验中,高酪组、低酪组和低复组潜伏时间和空白对照组相当,明显低于晕船组和其他干预组(P＜0.05).结论 低剂量支链氨基酸、酪氨酸复合配方对促进晕船刺激后大鼠脑体疲劳的快速恢复效果最佳.

Objective To investigate the changes of 5-HT2A receptor mRNA in rat vestibular nuclei during the adaptation of sea-sickness. Methods 40 SD rats were randomly distributed into five groups: control group, motion-sickness stimulation groups of 1-day, 3-day, 7-day and 14-day. Sea-sickness stimulation on rats was imitated by crampton facility, and vestibular nuclei were distracted according to the rat brain map. Real-time fluorescence quantitative PCR with SYBR GreenⅠtechnique was taken to detect the changes of 5-HT2A mRNA expression level. Results 5-HT2A receptor mRNA relative expression levels of sea-sickness 1-, 3-, 7-and 14-day groups were 3.35, 3.54, 1.23 and 1.02 times higher than those of the control group respectively. The levels of 5-HT2A receptor mRNA expression of sea-sickness significantly enhanced and kept high in the first and third day, and returned to the regular levels in the seventh day. Conclusion Sea-sickness stimulation might induce the enhance of 5-HT2A receptor mRNA in rat vestibular nuclei.