The Japanese journal of physiology最新文献

{"title":"Modelling unitary fields and the single‐neuron contribution to local field potentials in the hippocampus","authors":"Maria Teleńczuk, B. Teleńczuk, A. Destexhe","doi":"10.1101/602953","DOIUrl":"https://doi.org/10.1101/602953","url":null,"abstract":"Synaptic currents represent a major contribution to the local field potential (LFP) in brain tissue, but the respective contribution of excitatory and inhibitory synapses is not known. Here, we provide estimates of this contribution by using computational models of hippocampal pyramidal neurons, constrained by in vitro recordings. We focus on the unitary LFP (uLFP) generated by single neurons in the CA3 region of the hippocampus. We first reproduce experimental results for hippocampal basket cells, and in particular how inhibitory uLFP are distributed within hippocampal layers. Next, we calculate the uLFP generated by pyramidal neurons, using morphologically-reconstructed CA3 pyramidal cells. The model shows that the excitatory uLFP is of small amplitude, smaller than inhibitory uLFPs. Indeed, when the two are simulated together, inhibitory uLFPs mask excitatory uLFPs, which might create the illusion that the inhibitory field is generated by pyramidal cells. These results provide an explanation for the observation that excitatory and inhibitory uLFPs are of the same polarity, in vivo and in vitro. These results also show that somatic inhibitory currents are large contributors of the LFP, which is important information to interpret this signal. Finally, the results of our model might form the basis of a simple method to compute the LFP, which could be applied to point neurons for each cell type, thus providing a simple biologically-grounded method to calculate LFPs from neural networks.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"21 1","pages":"3957 - 3972"},"PeriodicalIF":0.0,"publicationDate":"2019-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84986642","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}

{"title":"The Effects of Drugs and other Agencies upon the Respiratory Movements","authors":"H. Wood","doi":"10.1113/jphysiol.1892.sp000438","DOIUrl":"https://doi.org/10.1113/jphysiol.1892.sp000438","url":null,"abstract":"","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"64 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88141603","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}

{"title":"Fetal adaptations in insulin secretion result from high catecholamines during placental insufficiency","authors":"S. Limesand, P. Rozance","doi":"10.1113/JP273324","DOIUrl":"https://doi.org/10.1113/JP273324","url":null,"abstract":"Placental insufficiency and intrauterine growth restriction (IUGR) of the fetus affects approximately 8% of all pregnancies and is associated with short‐ and long‐term disturbances in metabolism. In pregnant sheep, experimental models with a small, defective placenta that restricts delivery of nutrients and oxygen to the fetus result in IUGR. Low blood oxygen concentrations increase fetal plasma catecholamine concentrations, which lower fetal insulin concentrations. All of these observations in sheep models with placental insufficiency are consistent with cases of human IUGR. We propose that sustained high catecholamine concentrations observed in the IUGR fetus produce developmental adaptations in pancreatic β‐cells that impair fetal insulin secretion. Experimental evidence supporting this hypothesis shows that chronic elevation in circulating catecholamines in IUGR fetuses persistently inhibits insulin concentrations and secretion. Elevated catecholamines also allow for maintenance of a normal fetal basal metabolic rate despite low fetal insulin and glucose concentrations while suppressing fetal growth. Importantly, a compensatory augmentation in insulin secretion occurs following inhibition or cessation of catecholamine signalling in IUGR fetuses. This finding has been replicated in normally grown sheep fetuses following a 7‐day noradrenaline (norepinephrine) infusion. Together, these programmed effects will potentially create an imbalance between insulin secretion and insulin‐stimulated glucose utilization in the neonate which probably explains the transient hyperinsulinism and hypoglycaemia in some IUGR infants.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"148 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77787454","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}

{"title":"Dietary interventions for fetal growth restriction – therapeutic potential of dietary nitrate supplementation in pregnancy","authors":"E. Cottrell, T. Tropea, L. Ormesher, S. Greenwood, M. Wareing, E. Johnstone, J. Myers, C. Sibley","doi":"10.1113/JP273331","DOIUrl":"https://doi.org/10.1113/JP273331","url":null,"abstract":"Fetal growth restriction (FGR) affects around 5% of pregnancies and is associated with significant short‐ and long‐term adverse outcomes. A number of factors can increase the risk of FGR, one of which is poor maternal diet. In terms of pathology, both clinically and in many experimental models of FGR, impaired uteroplacental vascular function is implicated, leading to a reduction in the delivery of oxygen and nutrients to the developing fetus. Whilst mechanisms underpinning impaired uteroplacental vascular function are not fully understood, interventions aimed at enhancing nitric oxide (NO) bioavailability remain a key area of interest in obstetric research. In addition to endogenous NO production from the amino acid l‐arginine, via nitric oxide synthase (NOS) enzymes, research in recent years has established that significant NO can be derived from dietary nitrate, via the ‘alternative NO pathway’. Dietary nitrate, abundant in green leafy vegetables and beetroot, can increase NO bioactivity, conferring beneficial effects on cardiovascular function and blood flow. Given the beneficial effects of dietary nitrate supplementation to date in non‐pregnant humans and animals, current investigations aim to assess the therapeutic potential of this approach in pregnancy to enhance NO bioactivity, improve uteroplacental vascular function and increase fetal growth.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74157282","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}

{"title":"Rapid frequency‐dependent changes in free mitochondrial calcium concentration in rat cardiac myocytes","authors":"R. C. Wüst, M. Helmes, Jody L. Martin, Thomas J. T. Van der Wardt, R. Musters, J. van der Velden, G. Stienen","doi":"10.1113/JP273589","DOIUrl":"https://doi.org/10.1113/JP273589","url":null,"abstract":"Calcium ions regulate mitochondrial ATP production and contractile activity and thus play a pivotal role in matching energy supply and demand in cardiac muscle. The magnitude and kinetics of the changes in free mitochondrial calcium concentration in cardiac myocytes are largely unknown. Rapid stimulation frequency‐dependent increases but relatively slow decreases in free mitochondrial calcium concentration were observed in rat cardiac myocytes. This asymmetry caused a rise in the mitochondrial calcium concentration with stimulation frequency. These results provide insight into the mechanisms of mitochondrial calcium uptake and release that are important in healthy and diseased myocardium.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"45 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79305905","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}

{"title":"Non‐chemosensitive parafacial neurons simultaneously regulate active expiration and airway patency under hypercapnia in rats","authors":"Alan A de Britto, D. Moraes","doi":"10.1113/JP273335","DOIUrl":"https://doi.org/10.1113/JP273335","url":null,"abstract":"Hypercapnia or parafacial respiratory group (pFRG) disinhibition at normocapnia evokes active expiration in rats by recruitment of pFRG late‐expiratory (late‐E) neurons. We show that hypercapnia simultaneously evoked active expiration and exaggerated glottal dilatation by late‐E synaptic excitation of abdominal, hypoglossal and laryngeal motoneurons. Simultaneous rhythmic expiratory activity in previously silent pFRG late‐E neurons, which did not express the marker of ventral medullary CO2‐sensitive neurons (transcription factor Phox2b), was also evoked by hypercapnia. Hypercapnia‐evoked active expiration, neural and neuronal late‐E activities were eliminated by pFRG inhibition, but not after blockade of synaptic excitation. Hypercapnia produces disinhibition of non‐chemosensitive pFRG late‐E neurons to evoke active expiration and concomitant cranial motor respiratory responses controlling the oropharyngeal and upper airway patency.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90880518","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}

{"title":"Characterizing the sympatholytic role of endothelial‐dependent vasodilator signalling during handgrip exercise","authors":"Iain R Lamb, N. Novielli","doi":"10.1113/JP273806","DOIUrl":"https://doi.org/10.1113/JP273806","url":null,"abstract":"The dynamic metabolic range of skeletal muscle necessitates an equally dynamic blood flow requirement, to the point where the demand for skeletal muscle blood flow during intense bouts of large muscle mass exercise can theoretically ‘outstrip’ the heart's ability to generate the cardiac output necessary for maintaining sufficient mean arterial pressure (MAP) and muscle perfusion. \u0000 \u0000This article is protected by copyright. All rights reserved","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85312811","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}

{"title":"Do changes in mitochondrial quality contribute to increases in skeletal muscle oxidative capacity following endurance training?","authors":"M. Bartlett, Julia D. Miehm, Liam F. Fitzgerald, C. Straight","doi":"10.1113/JP273809","DOIUrl":"https://doi.org/10.1113/JP273809","url":null,"abstract":"Endurance training improves skeletal muscle oxidative capacity, but the molecular adaptations that drive this process are not fully understood. Specifically, whether oxidative capacity is improved solely by augmentations in mitochondrial quantity, or by enhanced mitochondrial quality as well, is unclear. For example, compared to active individuals, elite endurance athletes exhibit superior in vitro oxidative capacity even when normalised to citrate synthase (CS) activity, a common marker of mitochondrial quantity (Jacobs & Lundby, 2013). Two important questions emerge from these results: (1) what molecular or enzymatic aspects of mitochondrial composition might allow rates of in vitro oxidative capacity to increase for a given mitochondrial volume, and (2) what endurance training methods are best suited to stimulate these positive adaptations? Adaptations to endurance training have traditionally been studied following a period of moderate intensity continuous training (MICT), which is characterised by prolonged periods of aerobic activity at submaximal workloads (i.e. high volume training). More recently, interest has shifted towards high intensity interval training (HIIT), which involves repeated bouts of vigorous-intensity exercise interspersed with periods of recovery. Daussin et al. (2008) reported that in vitro oxidative capacity is significantly improved by HIIT, but not by MICT. Larsen et al. (2013) demonstrated that as few as six sessions of HIIT are sufficient to improve in vivo markers of skeletal muscle oxidative capacity, measured as the maximal rate of phosphocreatine resynthesis. However, these studies did not “normalise” oxidative capacity measurements to mitochondrial quantity, nor did they measure changes in mitochondrial enzymatic composition, making it difficult to infer the molecular mechanisms that control measures of oxidative capacity and how training intensity may influence these changes. In an article in The Journal of Physiology, MacInnis et al. (2016) attempted to address this gap in the literature by comparing changes in whole muscle and mitochondria-specific in vitro oxidative capacity after 2 weeks of MICT and HIIT. To compare the different training modalities, they used single-leg cycle ergometry, which allowed all participants (n=10 young males) to perform both MICT and HIIT over the same training period and serve as their own controls. Peak aerobic capacity (Wpeak) was measured on each leg using a ramp protocol before and after 2 weeks of endurance training. Participants completed six sessions of single-leg MICT (30 min at 50% Wpeak) and HIIT (4 bouts of 5 min at 65% Wpeak and 2.5 min at 20% Wpeak). Muscle biopsies were taken from the vastus lateralis of each leg preand post-training to measure markers of mitochondrial composition and mitochondrial oxidative capacity. Markers of mitochondrial composition included CS (used as a marker for mitochondrial quantity), cytochrome c oxidase subunit 4 (COXIV), NADH:ubiquin","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86062537","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}

{"title":"The quantal catecholamine release from mouse chromaffin cells challenged with repeated ACh pulses is regulated by the mitochondrial Na+/Ca2+ exchanger","authors":"Ángela López-Gil, Carmen Nanclares, I. Méndez-López, Carmen Martínez-Ramírez, C. de los Ríos, J. F. Padín-Nogueira, M. Montero, L. Gandía, Antonio G. García","doi":"10.1113/JP273339","DOIUrl":"https://doi.org/10.1113/JP273339","url":null,"abstract":"Upon repeated application of short ACh pulses to C57BL6J mouse chromaffin cells, the amperometrically monitored secretory responses promptly decayed to a steady‐state level of around 25% of the initial response. A subsequent K+ pulse, however, overcame such decay. These data suggest that mouse chromaffin cells have a ready release‐vesicle pool that is selectively recruited by the physiological neurotransmitter ACh. The ACh‐sensitive vesicle pool is refilled and maintained by the rate of Ca2+ delivery from mitochondria to the cytosol, through the mitochondrial Na+/Ca2+ exchanger (mNCX). ITH12662, a novel blocker of the mNCX, prevented the decay of secretion elicited by ACh pulses and delayed the rate of [Ca2+]c clearance. This regulatory pathway may be physiologically relevant in situations of prolonged stressful conflicts where a sustained catecholamine release is regulated by mitochondrial Ca2+ circulation through the mNCX, which couples respiration and ATP synthesis to long‐term stimulation of chromaffin cells by endogenously released ACh.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"&NA; 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83450996","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}

{"title":"Bicarbonate‐rich fluid secretion predicted by a computational model of guinea‐pig pancreatic duct epithelium","authors":"M. Yamaguchi, M. Steward, Kieran Smallbone, Y. Sohma, A. Yamamoto, S. Ko, T. Kondo, H. Ishiguro","doi":"10.1113/JP273306","DOIUrl":"https://doi.org/10.1113/JP273306","url":null,"abstract":"The ductal system of the pancreas secretes large volumes of alkaline fluid containing HCO3− concentrations as high as 140 mm during hormonal stimulation. A computational model has been constructed to explore the underlying ion transport mechanisms. Parameters were estimated by fitting the model to experimental data from guinea‐pig pancreatic ducts. The model was readily able to secrete 140 mm HCO3−. Its capacity to do so was not dependent upon special properties of the cystic fibrosis transmembrane conductance regulator (CFTR) anion channels and solute carrier family 26 member A6 (SLC26A6) anion exchangers. We conclude that the main requirement for secreting high HCO3− concentrations is to minimize the secretion of Cl− ions. These findings help to clarify the mechanism responsible for pancreatic HCO3− secretion, a vital process that prevents the formation of protein plugs and viscous mucus in the ducts, which could otherwise lead to pancreatic disease.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"48 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80604842","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}