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Advanced glycation end products promote ROS production via PKC/p47 phox axis in skeletal muscle cells. 高级糖化终产物通过 PKC/p47 phox 轴促进骨骼肌细胞产生 ROS。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-10-05 DOI: 10.1186/s12576-024-00944-1
Shinichiro Suzuki, Tatsuya Hayashi, Tatsuro Egawa
{"title":"Advanced glycation end products promote ROS production via PKC/p47 phox axis in skeletal muscle cells.","authors":"Shinichiro Suzuki, Tatsuya Hayashi, Tatsuro Egawa","doi":"10.1186/s12576-024-00944-1","DOIUrl":"https://doi.org/10.1186/s12576-024-00944-1","url":null,"abstract":"<p><p>Advanced glycation end products (AGEs) are risk factors for various diseases, including sarcopenia. One of the deleterious effects of AGEs is the induction of abnormal reactive oxygen species (ROS) production in skeletal muscle. However, the underlying mechanism remains poorly understood. Therefore, the aim of this study was to elucidate how AGEs induce ROS production in skeletal muscle cells. This study demonstrated that AGEs treatment promoted ROS production in myoblasts and myotubes while PKC inhibitor abolished ROS production by AGEs stimulation. Phosphorylation of p47 phox by kinases such as PKCα is required to form the Nox2 complex, which induces ROS production. In this study, AGEs treatment promoted the phosphorylation of PKCα and p47 phox in myoblasts and myotubes. Our findings suggest that AGEs promote ROS production through the phosphorylation of PKCα and p47 phox in skeletal muscle cells.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Thermosensing ability of TRPC5: current knowledge and unsettled questions. TRPC5 的热感应能力:现有知识和悬而未决的问题。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-10-03 DOI: 10.1186/s12576-024-00942-3
Alexandra Ptakova, Viktorie Vlachova
{"title":"Thermosensing ability of TRPC5: current knowledge and unsettled questions.","authors":"Alexandra Ptakova, Viktorie Vlachova","doi":"10.1186/s12576-024-00942-3","DOIUrl":"10.1186/s12576-024-00942-3","url":null,"abstract":"<p><p>Our understanding of how the mammalian somatosensory system detects noxious cold is still limited. While the role of TRPM8 in signaling mild non-noxious coolness is reasonably understood, the molecular identity of channels transducing painful cold stimuli remains unresolved. TRPC5 was originally described to contribute to moderate cold responses of dorsal root ganglia neurons in vitro, but mice lacking TRPC5 exhibited no change in behavioral responses to cold temperature. The question of why a channel endowed with the ability to be activated by cooling contributes to the cold response only under certain conditions is currently being intensively studied. It seems increasingly likely that the physiological detection of cold temperatures involves multiple different channels and mechanisms that modulate the threshold and intensity of perception. In this review, we aim to outline how TRPC5 may contribute to these mechanisms and what molecular features are important for its role as a cold sensor.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Acupuncture improves spatial learning and memory impairment caused by herpes simplex virus type-1 in rats through the p38 MAPK/CREB pathway. 针灸可通过 p38 MAPK/CREB 通路改善 1 型单纯疱疹病毒导致的大鼠空间学习和记忆损伤。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-10-03 DOI: 10.1186/s12576-024-00941-4
Hongjiao Jin, Rui Huang, Zhu Li, Mi Liu, Ning Zhao, Haiyan Zhang, Yong Lin
{"title":"Acupuncture improves spatial learning and memory impairment caused by herpes simplex virus type-1 in rats through the p38 MAPK/CREB pathway.","authors":"Hongjiao Jin, Rui Huang, Zhu Li, Mi Liu, Ning Zhao, Haiyan Zhang, Yong Lin","doi":"10.1186/s12576-024-00941-4","DOIUrl":"10.1186/s12576-024-00941-4","url":null,"abstract":"<p><strong>Background: </strong>Acupuncture can improve herpes simplex encephalitis (HSE), but the underlying mechanism is not clear. Therefore, we evaluated the cognitive function and apoptosis in hippocampus caused by herpes simplex virus type-1 (HSV-1) in rats after acupuncture and described the molecular mechanism.</p><p><strong>Methods: </strong>Sprague-Dawley rats were induced into HSE models by HSV-1 infection. After 3 days, they received acupuncture at the acupoints of Xuanzhong (GB39), Baihui (GV20), Shenmen (HT7), Shenting (GV24), and Sanyinjiao (SP6), and/or intraperitoneal injection of the p38 MAPK inhibitor SB203580. Morris water maze test was performed on rats. The hippocampus of rats was obtained, and the expression of apoptosis-related genes in the tissues was detected by qRT-PCR. In addition, apoptosis-related proteins and proteins related to the p38 MAPK/CREB pathway in the tissues was detected by western blot.</p><p><strong>Results: </strong>After HSV-1 induction, the rat's escape latency was increased, the time spent on the platform in the target quadrant and the number of platform crossings significantly decreased. In addition, there was an increase in apoptosis in the hippocampus, accompanied by elevated levels of p-p38 and decreased levels of p-CREB. However, these effects could be improved by acupuncture treatment. Interestingly, SB203580 plays a similar role to acupuncture, and acupuncture could further enhance the impacts of SB203580 on cognitive function and apoptosis in hippocampus in HSE rats.</p><p><strong>Conclusion: </strong>Acupuncture improves spatial learning and memory impairment caused by HSV-1 in rats. The functional mechanism of acupuncture may be through the p38 MAPK/CREB pathway.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Acute effects of empagliflozin on open-loop baroreflex function and urine output in streptozotocin-induced type 1 diabetic rats. empagliflozin对链脲佐菌素诱导的1型糖尿病大鼠开环气压反射功能和尿量的急性影响
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-09-28 DOI: 10.1186/s12576-024-00938-z
Toru Kawada, Hiromi Yamamoto, Masafumi Fukumitsu, Takuya Nishikawa, Hiroki Matsushita, Yuki Yoshida, Kei Sato, Hidetaka Morita, Joe Alexander, Keita Saku
{"title":"Acute effects of empagliflozin on open-loop baroreflex function and urine output in streptozotocin-induced type 1 diabetic rats.","authors":"Toru Kawada, Hiromi Yamamoto, Masafumi Fukumitsu, Takuya Nishikawa, Hiroki Matsushita, Yuki Yoshida, Kei Sato, Hidetaka Morita, Joe Alexander, Keita Saku","doi":"10.1186/s12576-024-00938-z","DOIUrl":"https://doi.org/10.1186/s12576-024-00938-z","url":null,"abstract":"<p><p>Although sympathetic suppression is considered one of the mechanisms for cardioprotection afforded by sodium-glucose cotransporter 2 (SGLT2) inhibitors, whether SGLT2 inhibition acutely modifies sympathetic arterial pressure (AP) regulation remains unclear. We examined the acute effect of an SGLT2 inhibitor, empagliflozin (10 mg/kg), on open-loop baroreflex static characteristics in streptozotocin (STZ)-induced type 1 diabetic and control (CNT) rats (n = 9 each). Empagliflozin significantly increased urine flow [CNT: 25.5 (21.7-31.2) vs. 55.9 (51.0-64.5), STZ: 83.4 (53.7-91.7) vs. 121.2 (57.0-136.0) μL·min<sup>-1</sup>·kg<sup>-1</sup>, median (1st-3rd quartiles), P < 0.001 for empagliflozin and STZ]. Empagliflozin decreased the minimum sympathetic nerve activity (SNA) [CNT: 15.7 (6.8-18.4) vs. 10.5 (2.9-19.0), STZ: 36.9 (25.7-54.9) vs. 32.8 (15.1-37.5) %, P = 0.021 for empagliflozin and P = 0.003 for STZ], but did not significantly affect the peripheral arc characteristics assessed by the SNA-AP relationship. Despite the significant increase in urine flow and changes in several baroreflex parameters, empagliflozin preserved the overall sympathetic AP regulation in STZ-induced diabetic rats. The lack of a significant change in the peripheral arc may minimize reflex sympathetic activation, thereby enhancing a cardioprotective benefit of empagliflozin.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11438138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Anekomochi glutinous rice provides low postprandial glycemic response by enhanced insulin action via GLP-1 release and vagal afferents activation. Anekomochi 糯米通过释放 GLP-1 和激活迷走神经传入增强胰岛素作用,从而降低餐后血糖反应。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-09-27 DOI: 10.1186/s12576-024-00940-5
Kento Ohbayashi, Yudai Sugiyama, Taichi Nohmi, Kazusa Nishimura, Tetsuya Nakazaki, Yo-Ichiro Sato, Takehiro Masumura, Yusaku Iwasaki
{"title":"Anekomochi glutinous rice provides low postprandial glycemic response by enhanced insulin action via GLP-1 release and vagal afferents activation.","authors":"Kento Ohbayashi, Yudai Sugiyama, Taichi Nohmi, Kazusa Nishimura, Tetsuya Nakazaki, Yo-Ichiro Sato, Takehiro Masumura, Yusaku Iwasaki","doi":"10.1186/s12576-024-00940-5","DOIUrl":"https://doi.org/10.1186/s12576-024-00940-5","url":null,"abstract":"<p><p>Glutinous rice (mochi rice), compared to non-glutinous rice (uruchi rice), exhibits a wide range of glycemic index (GI) values, from low to high. However, the underlying mechanisms behind the variation in GI values remain poorly understood. In this study, we aimed to identify rice cultivars with a low postprandial glycemic response and investigate the mechanisms, focusing on insulin and incretin hormones. We examined seven glutinous rice cultivars and three non-glutinous rice cultivars. We discovered that Anekomochi, a glutinous rice cultivar, has the lowest postprandial glycemic response. Anekomochi significantly enhanced glucagon-like peptide-1 (GLP-1) secretion while suppressing insulin secretion. These effects were completely blunted by inhibiting GLP-1 receptor signaling and denervating the common hepatic branch of vagal afferent nerves that are crucial for sensing intestinal GLP-1. Our findings demonstrate that Anekomochi markedly enhances insulin action via GLP-1 release and vagal afferent neural pathways, thereby leading to a lower postprandial glycemic response.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11428336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders. 免疫检查点阻断疗法在老年相关神经退行性疾病中的局限性和潜在策略。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-09-23 DOI: 10.1186/s12576-024-00933-4
Noha N Lasheen, Salma Allam, Abdullrahman Elgarawany, Darin W Aswa, Rana Mansour, Ziad Farouk
{"title":"Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders.","authors":"Noha N Lasheen, Salma Allam, Abdullrahman Elgarawany, Darin W Aswa, Rana Mansour, Ziad Farouk","doi":"10.1186/s12576-024-00933-4","DOIUrl":"10.1186/s12576-024-00933-4","url":null,"abstract":"<p><p>Neurological disorders such as Alzheimer's disease (AD), and Parkinson's disease (PD) have no disease-modifying treatments, resulting in a global dementia crisis that affects more than 50 million people. Amyloid-beta (Aβ), tau, and alpha-synuclein (α-Syn) are three crucial proteins that are involved in the pathogenesis of these age-related neurodegenerative diseases. Only a few approved AD medications have been used in the clinic up to this point, and their results are only partial symptomatic alleviation for AD patients and cannot stop the progression of AD. Immunotherapies have attracted considerable interest as they target certain protein strains and conformations as well as promote clearance. Immunotherapies also have the potential to be neuroprotective: as they limit synaptic damage and spread of neuroinflammation by neutralizing extracellular protein aggregates. Lately, disease-modifying therapies (DMTs) that can alter the pathophysiology that underlies AD with anti-Aβ monoclonal antibodies (MAbs) (e.g., aducanumab, lecanemab, gantenerumab, donanemab, solanezumab, crenezumab, tilavonemab). Similarly, in Parkinson's disease (PD), DMTs utilizing anti-αSyn (MAbs) (e.g., prasinezumab, cinpanemab,) are progressively being developed and evaluated in clinical trials. These therapies are based on the hypothesis that both AD and PD may involve systemic impairments in cell-dependent clearance mechanisms of amyloid-beta (Aβ) and alpha-synuclein (αSyn), respectively, meaning the body's overall inability to effectively remove Aβ and αSyn due to malfunctioning cellular mechanisms. In this review we will provide possible evidence behind the use of immunotherapy with MAbs in AD and PD and highlight the recent clinical development landscape of anti-Aβ (MAbs) and anti-αSyn (MAbs) from these clinical trials in order to better investigate the therapeutic possibilities and adverse effects of these anti-Aβ and anti-αSyn MAbs on AD and PD.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11421184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of the central nervous system in cell non-autonomous signaling mechanisms of aging and longevity in mammals. 中枢神经系统在哺乳动物衰老和长寿的细胞非自主信号机制中的作用。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-08-31 DOI: 10.1186/s12576-024-00934-3
Takuya Urushihata, Akiko Satoh
{"title":"Role of the central nervous system in cell non-autonomous signaling mechanisms of aging and longevity in mammals.","authors":"Takuya Urushihata, Akiko Satoh","doi":"10.1186/s12576-024-00934-3","DOIUrl":"10.1186/s12576-024-00934-3","url":null,"abstract":"<p><p>Multiple organs orchestrate the maintenance of proper physiological function in organisms throughout their lifetimes. Recent studies have uncovered that aging and longevity are regulated by cell non-autonomous signaling mechanisms in several organisms. In the brain, particularly in the hypothalamus, aging and longevity are regulated by such cell non-autonomous signaling mechanisms. Several hypothalamic neurons have been identified as regulators of mammalian longevity, and manipulating them promotes lifespan extension or shortens the lifespan in rodent models. The hypothalamic structure and function are evolutionally highly conserved across species. Thus, elucidation of hypothalamic function during the aging process will shed some light on the mechanisms of aging and longevity and, thereby benefiting to human health.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11365208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The influence of exercise intensity on comorbid anxious behavior in psychiatric conditions. 运动强度对精神病患者合并焦虑行为的影响。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-08-02 DOI: 10.1186/s12576-024-00930-7
Dong-Joo Hwang, Tae-Kyung Kim
{"title":"The influence of exercise intensity on comorbid anxious behavior in psychiatric conditions.","authors":"Dong-Joo Hwang, Tae-Kyung Kim","doi":"10.1186/s12576-024-00930-7","DOIUrl":"10.1186/s12576-024-00930-7","url":null,"abstract":"<p><p>Many experts have extensively studied the potential of exercise as a treatment option for psychiatric conditions, including depression and autism spectrum disorder (ASD). Despite their core symptoms, these conditions exhibits comparable component traits, an anxiety. In this study, we explored the effect of exercise on behavioral abnormalities in psychiatric conditions, focusing on its intensity and emotional resilience. Shank3B knockout (KO<sup>SED</sup>) mice displaying self-injurious repetitive behavior and C57BL/6J mice, susceptible to stress as ASD and depression model, respectively, were subjected to moderate-intensity exercise (ME) for 2 weeks. ME mitigated the core symptoms (excessive grooming traits and behavioral despair) but did not exert a significant anxiolytic effect. Notably, exercise intensity has emerged as a critical determinant of its efficacy, as evidenced by a lower ventilation threshold and anxiolytic effect mediated by low-intensity exercise. The findings substantiate the notion that exercise is promising as a disease-modifying treatment, but intensity matters for emotional resilience.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11295499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Age-related alteration of the involvement of CD36 for salivary secretion from the parotid gland in mice. CD36参与小鼠腮腺唾液分泌与年龄有关的变化
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-07-29 DOI: 10.1186/s12576-024-00931-6
Keitaro Satoh, Yuta Ohno, Haruna Nagase, Masanori Kashimata, Kazunori Adachi
{"title":"Age-related alteration of the involvement of CD36 for salivary secretion from the parotid gland in mice.","authors":"Keitaro Satoh, Yuta Ohno, Haruna Nagase, Masanori Kashimata, Kazunori Adachi","doi":"10.1186/s12576-024-00931-6","DOIUrl":"10.1186/s12576-024-00931-6","url":null,"abstract":"<p><p>This in vivo mouse model study was conducted to investigate the temporal alteration of the function of CD36 in salivary secretion. CD36 was highly expressed in the parotid gland of BALB/c mice. No significant variations were shown in the CD36 levels in the 8-, 48-, and 72-week-old animals. However, pilocarpine-induced salivary secretion was reduced in an age-dependent manner, showing a significantly low level at the age of 72 weeks. Pilocarpine-induced salivary secretion was significantly reduced by pretreatment with a CD36 inhibitor at 8 and 48 weeks, but not at 72 weeks. In senescence-accelerated mice (SAM), the pilocarpine-induced salivary secretion was significantly reduced at the age of 56 weeks, and a significantly lower amount of CD36 was demonstrated in the parotid gland, compared with the control. These results suggest that the involvement of parotid CD36 in mouse salivary secretion is altered with age.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11285320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Microglia mediate the increase in slow-wave sleep associated with high ambient temperature. 小胶质细胞介导了与高环境温度相关的慢波睡眠的增加。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2024-07-17 DOI: 10.1186/s12576-024-00929-0
Sena Hatori, Futaba Matsui, Zhiwen Zhou, Hiroaki Norimoto
{"title":"Microglia mediate the increase in slow-wave sleep associated with high ambient temperature.","authors":"Sena Hatori, Futaba Matsui, Zhiwen Zhou, Hiroaki Norimoto","doi":"10.1186/s12576-024-00929-0","DOIUrl":"10.1186/s12576-024-00929-0","url":null,"abstract":"<p><p>An increase in ambient temperature leads to an increase in sleep. However, the mechanisms behind this phenomenon remain unknown. This study aimed to investigate the role of microglia in the increase of sleep caused by high ambient temperature. We confirmed that at 35 °C, slow-wave sleep was significantly increased relative to those observed at 25 °C. Notably, this effect was abolished upon treatment with PLX3397, a CSF1R inhibitor that can deplete microglia, while sleep amount at 25 °C was unaffected. These observations suggest that microglia play a pivotal role in modulating the homeostatic regulation of sleep in response to the fluctuations in ambient temperature.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11253348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141633835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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