{"title":"The human physiological impact of global deoxygenation.","authors":"Daniel Martin, Helen McKenna, Valerie Livina","doi":"10.1007/s12576-016-0501-0","DOIUrl":"10.1007/s12576-016-0501-0","url":null,"abstract":"<p><p>There has been a clear decline in the volume of oxygen in Earth's atmosphere over the past 20 years. Although the magnitude of this decrease appears small compared to the amount of oxygen in the atmosphere, it is difficult to predict how this process may evolve, due to the brevity of the collected records. A recently proposed model predicts a non-linear decay, which would result in an increasingly rapid fall-off in atmospheric oxygen concentration, with potentially devastating consequences for human health. We discuss the impact that global deoxygenation, over hundreds of generations, might have on human physiology. Exploring the changes between different native high-altitude populations provides a paradigm of how humans might tolerate worsening hypoxia over time. Using this model of atmospheric change, we predict that humans may continue to survive in an unprotected atmosphere for ~3600 years. Accordingly, without dramatic changes to the way in which we interact with our planet, humans may lose their dominance on Earth during the next few millennia.</p>","PeriodicalId":22836,"journal":{"name":"The Journal of Physiological Sciences","volume":"40 1","pages":"97-106"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5138252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78488685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuronal circuits and physiological roles of the basal ganglia in terms of transmitters, receptors and related disorders.","authors":"Katsuya Yamada, Susumu Takahashi, Fuyuki Karube, Fumino Fujiyama, Kazuto Kobayashi, Akinori Nishi, Toshihiko Momiyama","doi":"10.1007/s12576-016-0445-4","DOIUrl":"10.1007/s12576-016-0445-4","url":null,"abstract":"<p><p>The authors have reviewed recent research advances in basal ganglia circuitry and function, as well as in related disorders from multidisciplinary perspectives derived from the results of morphological, electrophysiological, behavioral, biochemical and molecular biological studies. Based on their expertise in their respective fields, as denoted in the text, the authors discuss five distinct research topics, as follows: (1) area-specific dopamine receptor expression of astrocytes in basal ganglia, (2) the role of physiologically released dopamine in the striatum, (3) control of behavioral flexibility by striatal cholinergic interneurons, (4) regulation of phosphorylation states of DARPP-32 by protein phosphatases and (5) physiological perspective on deep brain stimulation with optogenetics and closed-loop control for ameliorating parkinsonism.</p>","PeriodicalId":22836,"journal":{"name":"The Journal of Physiological Sciences","volume":"11 1","pages":"435-446"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84589883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Somato-axodendritic release of oxytocin into the brain due to calcium amplification is essential for social memory.","authors":"Haruhiro Higashida","doi":"10.1007/s12576-015-0425-0","DOIUrl":"10.1007/s12576-015-0425-0","url":null,"abstract":"<p><p>Oxytocin (OT) is released into the brain from the cell soma, axons, and dendrites of neurosecretory cells in the hypothalamus. Locally released OT can activate OT receptors, form inositol-1,4,5-trisphosphate and elevate intracellular free calcium (Ca(2+)) concentrations [(Ca(2+)) i ] in self and neighboring neurons in the hypothalamus, resulting in further OT release: i.e., autocrine or paracrine systems of OT-induced OT release. CD38-dependent cyclic ADP-ribose (cADPR) is also involved in this autoregulation by elevating [Ca(2+)] i via Ca(2+) mobilization through ryanodine receptors on intracellular Ca(2+) pools that are sensitive to both Ca(2+) and cADPR. In addition, it has recently been reported that heat stimulation and hyperthermia enhance [Ca(2+)] i increases by Ca(2+) influx, probably through TRPM2 cation channels, suggesting that cADPR and TRPM2 molecules act as Ca(2+) signal amplifiers. Thus, OT release is not simply due to depolarization-secretion coupling. Both of these molecules play critical roles not only during labor and milk ejection in reproductive females, but also during social behavior in daily life in both genders. This was clearly demonstrated in CD38 knockout mice in that social behavior was impaired by reduction of [Ca(2+)] i elevation and subsequent OT secretion. Evidence for the associations of CD38 with social behavior and psychiatric disorder is discussed, especially in subjects with autism spectrum disorder. </p>","PeriodicalId":22836,"journal":{"name":"The Journal of Physiological Sciences","volume":"1 1","pages":"275-82"},"PeriodicalIF":0.0,"publicationDate":"2016-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4893072/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84874566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neural stem cells and neuro/gliogenesis in the central nervous system: understanding the structural and functional plasticity of the developing, mature, and diseased brain.","authors":"Masahiro Yamaguchi, Tatsunori Seki, Itaru Imayoshi, Nobuaki Tamamaki, Yoshitaka Hayashi, Yoshitaka Tatebayashi, Seiji Hitoshi","doi":"10.1007/s12576-015-0421-4","DOIUrl":"10.1007/s12576-015-0421-4","url":null,"abstract":"<p><p>Neurons and glia in the central nervous system (CNS) originate from neural stem cells (NSCs). Knowledge of the mechanisms of neuro/gliogenesis from NSCs is fundamental to our understanding of how complex brain architecture and function develop. NSCs are present not only in the developing brain but also in the mature brain in adults. Adult neurogenesis likely provides remarkable plasticity to the mature brain. In addition, recent progress in basic research in mental disorders suggests an etiological link with impaired neuro/gliogenesis in particular brain regions. Here, we review the recent progress and discuss future directions in stem cell and neuro/gliogenesis biology by introducing several topics presented at a joint meeting of the Japanese Association of Anatomists and the Physiological Society of Japan in 2015. Collectively, these topics indicated that neuro/gliogenesis from NSCs is a common event occurring in many brain regions at various ages in animals. Given that significant structural and functional changes in cells and neural networks are accompanied by neuro/gliogenesis from NSCs and the integration of newly generated cells into the network, stem cell and neuro/gliogenesis biology provides a good platform from which to develop an integrated understanding of the structural and functional plasticity that underlies the development of the CNS, its remodeling in adulthood, and the recovery from diseases that affect it. </p>","PeriodicalId":22836,"journal":{"name":"The Journal of Physiological Sciences","volume":"26 1","pages":"197-206"},"PeriodicalIF":0.0,"publicationDate":"2016-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73508046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Reciprocal effects of capsaicin and menthol on thermosensation through regulated activities of TRPV1 and TRPM8.","authors":"Masayuki Takaishi, Kunitoshi Uchida, Yoshiro Suzuki, Hiroshi Matsui, Tadashi Shimada, Fumitaka Fujita, Makoto Tominaga","doi":"10.1007/s12576-015-0427-y","DOIUrl":"10.1007/s12576-015-0427-y","url":null,"abstract":"<p><p>Transient receptor potential vanilloid 1 (TRPV1) is activated by elevated temperature (>42 °C), and it has been reported that cold temperature decreases capsaicin-induced TRPV1 activity. In contrast, transient receptor potential melastatin 8 (TRPM8) is activated by low temperatures and menthol, and heat stimulation suppresses menthol-evoked TRPM8 currents. These findings suggest that the effects of specific agents on TRPV1 and TRPM8 channels are intricately interrelated. We examined the effects of menthol on human (h)TRPV1 and of capsaicin on hTRPM8. hTRPV1 currents activated by heat and capsaicin were inhibited by menthol, whereas hTRPM8 currents activated by cold and menthol were similarly inhibited by capsaicin. An in vivo sensory irritation test showed that menthol conferred an analgesic effect on the sensory irritation evoked by a capsaicin analogue. These results indicate that in our study the agonists of TRPV1 and TRPM8 interacted with both of these channels and suggest that the anti-nociceptive effects of menthol can be partially explained by this phenomenon.</p>","PeriodicalId":22836,"journal":{"name":"The Journal of Physiological Sciences","volume":"82 1","pages":"143-55"},"PeriodicalIF":0.0,"publicationDate":"2016-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4752590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72711666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sleep as a biological problem: an overview of frontiers in sleep research.","authors":"Takeshi Kanda, Natsuko Tsujino, Eriko Kuramoto, Yoshimasa Koyama, Etsuo A Susaki, Sachiko Chikahisa, Hiromasa Funato","doi":"10.1007/s12576-015-0414-3","DOIUrl":"10.1007/s12576-015-0414-3","url":null,"abstract":"<p><p>Sleep is a physiological process not only for the rest of the body but also for several brain functions such as mood, memory, and consciousness. Nevertheless, the nature and functions of sleep remain largely unknown due to its extremely complicated nature and lack of optimized technology for the experiments. Here we review the recent progress in the biology of the mammalian sleep, which covers a wide range of research areas: the basic knowledge about sleep, the physiology of cerebral cortex in sleeping animals, the detailed morphological features of thalamocortical networks, the mechanisms underlying fluctuating activity of autonomic nervous systems during rapid eye movement sleep, the cutting-edge technology of tissue clearing for visualization of the whole brain, the ketogenesis-mediated homeostatic regulation of sleep, and the forward genetic approach for identification of novel genes involved in sleep. We hope this multifaceted review will be helpful for researchers who are interested in the biology of sleep. </p>","PeriodicalId":22836,"journal":{"name":"The Journal of Physiological Sciences","volume":"28 1","pages":"1-13"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89411618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"President’s Symposium","authors":"Raphael J. Sonenshein","doi":"10.1007/BF03405839","DOIUrl":"https://doi.org/10.1007/BF03405839","url":null,"abstract":"","PeriodicalId":22836,"journal":{"name":"The Journal of Physiological Sciences","volume":"44 1","pages":"S7-S10"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84552959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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