{"title":"Correction to: Persistent sodium currents in neurons: potential mechanisms and pharmacological blockers.","authors":"Peter Müller, Andreas Draguhn, Alexei V Egorov","doi":"10.1007/s00424-024-02995-0","DOIUrl":"10.1007/s00424-024-02995-0","url":null,"abstract":"","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1623"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141752355","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}
{"title":"Stability of N-type inactivation and the coupling between N-type and C-type inactivation in the Aplysia Kv1 channel.","authors":"Tokunari Iwamuro, Kazuki Itohara, Yasuo Furukawa","doi":"10.1007/s00424-024-02982-5","DOIUrl":"10.1007/s00424-024-02982-5","url":null,"abstract":"<p><p>The voltage-dependent potassium channels (Kv channels) show several different types of inactivation. N-type inactivation is a fast inactivating mechanism, which is essentially an open pore blockade by the amino-terminal structure of the channel itself or the auxiliary subunit. There are several functionally discriminatable slow inactivation (C-type, P-type, U-type), the mechanism of which is supposed to include rearrangement of the pore region. In some Kv1 channels, the actual inactivation is brought about by coupling of N-type and C-type inactivation (N-C coupling). In the present study, we focused on the N-C coupling of the Aplysia Kv1 channel (AKv1). AKv1 shows a robust N-type inactivation, but its recovery is almost thoroughly from C-type inactivated state owing to the efficient N-C coupling. In the I8Q mutant of AKv1, we found that the inactivation as well as its recovery showed two kinetic components apparently correspond to N-type and C-type inactivation. Also, the cumulative inactivation which depends on N-type mechanism in AKv1 was hindered in I8Q, suggesting that N-type inactivation of I8Q is less stable. We also found that Zn <math><msup><mrow></mrow> <mrow><mn>2</mn> <mo>+</mo></mrow> </msup> </math> specifically accelerates C-type inactivation of AKv1 and that H382 in the pore turret is involved in the Zn <math><msup><mrow></mrow> <mrow><mn>2</mn> <mo>+</mo></mrow> </msup> </math> binding. Because the region around Ile <math><msup><mrow></mrow> <mn>8</mn></msup> </math> (I8) in AKv1 has been suggested to be involved in the pre-block binding of the amino-terminal structure, our results strengthen a hypothesis that the stability of the pre-block state is important for stable N-type inactivation as well as the N-C coupling in the Kv1 channel inactivation.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1493-1516"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11639194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141617021","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}
Zsuzsa Radványi, Udo Schnitzbauer, Eva Maria Pastor-Arroyo, Simone Hölker, Nina Himmerkus, Markus Bleich, Dominik Müller, Tilman Breiderhoff, Nati Hernando, Carsten A Wagner
{"title":"Absence of claudin-3 does not alter intestinal absorption of phosphate in mice.","authors":"Zsuzsa Radványi, Udo Schnitzbauer, Eva Maria Pastor-Arroyo, Simone Hölker, Nina Himmerkus, Markus Bleich, Dominik Müller, Tilman Breiderhoff, Nati Hernando, Carsten A Wagner","doi":"10.1007/s00424-024-02998-x","DOIUrl":"10.1007/s00424-024-02998-x","url":null,"abstract":"<p><p>Intestinal absorption of phosphate is bimodal, consisting of a transcellular pathway and a poorly characterized paracellular mode, even though the latter one contributes to the bulk of absorption under normal dietary conditions. Claudin-3 (Cldn3), a tight junction protein present along the whole intestine in mice, has been proposed to tighten the paracellular pathway for phosphate. The aim of this work was to characterize the phosphate-related phenotype of Cldn3-deficient mice. Cldn3-deficient mice and wildtype littermates were fed standard diet or challenged for 3 days with high dietary phosphate. Feces, urine, blood, intestinal segments and kidneys were collected. Measurements included fecal, urinary, and plasma concentrations of phosphate and calcium, plasma levels of phosphate-regulating hormones, evaluation of trans- and paracellular phosphate transport across jejunum and ileum, and analysis of intestinal phosphate and calcium permeabilities. Fecal and urinary excretion of phosphate as well as its plasma concentration was similar in both genotypes, under standard and high-phosphate diet. However, Cldn3-deficient mice challenged with high dietary phosphate had a reduced urinary calcium excretion and increased plasma levels of calcitriol. Intact FGF23 concentration was also similar in both groups, regardless of the dietary conditions. We found no differences either in intestinal phosphate transport (trans- or paracellular) and phosphate and calcium permeabilities between genotypes. The intestinal expression of claudin-7 remained unaltered in Cldn3-deficient mice. Our data do not provide evidence for a decisive role of Cldn3 for intestinal phosphate absorption and phosphate homeostasis. In addition, our data suggest a novel role of Cldn3 in regulating calcitriol levels.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1597-1612"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141902594","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}
Christopher Gutierrez, Magdalena Peirone, Andrea Carranza, Guillermo Di Girolamo, Patricia Bonazzola, Rocío Castilla
{"title":"Mild hyperbaric oxygen exposure protects heart during ischemia/reperfusion and affects vascular relaxation.","authors":"Christopher Gutierrez, Magdalena Peirone, Andrea Carranza, Guillermo Di Girolamo, Patricia Bonazzola, Rocío Castilla","doi":"10.1007/s00424-024-02992-3","DOIUrl":"10.1007/s00424-024-02992-3","url":null,"abstract":"<p><p>Mild hyperbaric oxygen therapy (mHBOT) is an adjuvant therapy used in conditions where tissue oxygenation is reduced and is implemented using pressures less than 1.5 ATA and 100% O<sub>2</sub> (instead of the classical HBOT at 1.9-3 ATA) which results in cheaper, easier to implement, and equally effective. mHBOT is offered for wellness and beauty and as an anti-aging strategy, in spite of the absence of studies on the cardiovascular system. Consequently, we investigated the impact of mHBOT on the cardiovascular system. Mechanical and energetic parameters of isolated heart submitted to ischemia/reperfusion injury and arterial contractile response from mHBOT-exposed rats were evaluated. In the heart, mHBOT increased pre-ischemic velocity of contraction and ischemic end-diastolic pressure and developed pressure and contractile economy during reperfusion. mHBOT decreased infarct size and increased the plasma nitrite levels. In the artery, mHBOT increased acetylcholine sensitivity. mHBOT protects the heart during ischemia/reperfusion and affects vascular relaxation.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1587-1595"},"PeriodicalIF":4.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141760222","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}
{"title":"Effect of hypoxia on GLP-1 secretion - an in vitro study using enteroendocrine STC-1 -cells as a model.","authors":"Ravikant Sharma, Ghulam Shere Raza, Nalini Sodum, Jaroslaw Walkowiak, Karl-Heinz Herzig","doi":"10.1007/s00424-024-02996-z","DOIUrl":"10.1007/s00424-024-02996-z","url":null,"abstract":"<p><p>Glucagon-like peptide (GLP)-1 is a hormone released by enteroendocrine L-cells after food ingestion. L-cells express various receptors for nutrient sensing including G protein-coupled receptors (GPRs). Intestinal epithelial cells near the lumen have a lower O<sub>2</sub> tension than at the base of the crypts, which leads to hypoxia in L-cells. We hypothesized that hypoxia affects nutrient-stimulated GLP-1 secretion from the enteroendocrine cell line STC-1, the most commonly used model. In this study, we investigated the effect of hypoxia (1% O<sub>2</sub>) on alpha-linolenic acid (αLA) stimulated GLP-1 secretion and their receptor expressions. STC-1 cells were incubated for 12 h under hypoxia (1% O<sub>2</sub>) and treated with αLA to stimulate GLP-1 secretion. 12 h of hypoxia did not change basal GLP-1 secretion, but significantly reduced nutrient (αLA) stimulated GLP-1 secretion. In normoxia, αLA (12.5 μM) significantly stimulated (~ 5 times) GLP-1 secretion compared to control, but under hypoxia, GLP-1 secretion was reduced by 45% compared to normoxia. αLA upregulated GPR120, also termed free fatty acid receptor 4 (FFAR4), expressions under normoxia as well as hypoxia. Hypoxia downregulated GPR120 and GPR40 expression by 50% and 60%, respectively, compared to normoxia. These findings demonstrate that hypoxia does not affect the basal GLP-1 secretion but decreases nutrient-stimulated GLP-1 secretion. The decrease in nutrient-stimulated GLP-1 secretion was due to decreased GPR120 and GPR40 receptors expression. Changes in the gut environment and inflammation might contribute to the hypoxia of the epithelial and L-cells.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1613-1621"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141793045","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}
{"title":"Emerging connections between Piezo1 and BK channels in vascular smooth muscle cells.","authors":"Luigi Catacuzzeno, Antonio Michelucci","doi":"10.1007/s00424-024-03001-3","DOIUrl":"10.1007/s00424-024-03001-3","url":null,"abstract":"","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1475-1477"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141860466","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}
Sven Weidner, André Tomalka, Christian Rode, Tobias Siebert
{"title":"Impact of lengthening velocity on the generation of eccentric force by slow-twitch muscle fibers in long stretches.","authors":"Sven Weidner, André Tomalka, Christian Rode, Tobias Siebert","doi":"10.1007/s00424-024-02991-4","DOIUrl":"10.1007/s00424-024-02991-4","url":null,"abstract":"<p><p>After an initial increase, isovelocity elongation of a muscle fiber can lead to diminishing (referred to as Give in the literature) and subsequently increasing force. How the stretch velocity affects this behavior in slow-twitch fibers remains largely unexplored. Here, we stretched fully activated individual rat soleus muscle fibers from 0.85 to 1.3 optimal fiber length at stretch velocities of 0.01, 0.1, and 1 maximum shortening velocity, v<sub>max</sub>, and compared the results with those of rat EDL fast-twitch fibers obtained in similar experimental conditions. In soleus muscle fibers, Give was 7%, 18%, and 44% of maximum isometric force for 0.01, 0.1, and 1 v<sub>max</sub>, respectively. As in EDL fibers, the force increased nearly linearly in the second half of the stretch, although the number of crossbridges decreased, and its slope increased with stretch velocity. Our findings are consistent with the concept of a forceful detachment and subsequent crossbridge reattachment in the stretch's first phase and a strong viscoelastic titin contribution to fiber force in the second phase of the stretch. Interestingly, we found interaction effects of stretch velocity and fiber type on force parameters in both stretch phases, hinting at fiber type-specific differences in crossbridge and titin contributions to eccentric force. Whether fiber type-specific combined XB and non-XB models can explain these effects or if they hint at some not fully understood properties of muscle contraction remains to be shown. These results may stimulate new optimization perspectives in sports training and provide a better understanding of structure-function relations of muscle proteins.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1517-1527"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141752357","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}
Vera A Kulow, Robert Labes, Claudia S Czopek, Christian Rosenberger, Michael Fähling
{"title":"Galectin-3 protects distal convoluted tubules in rhabdomyolysis-induced kidney injury.","authors":"Vera A Kulow, Robert Labes, Claudia S Czopek, Christian Rosenberger, Michael Fähling","doi":"10.1007/s00424-024-02987-0","DOIUrl":"10.1007/s00424-024-02987-0","url":null,"abstract":"<p><p>Advanced glycation endproducts (AGEs) contribute to cellular damage of various pathologies, including kidney diseases. Acute kidney injury (AKI) represents a syndrome seldom characterized by a single, distinct pathophysiological cause. Rhabdomyolysis-induced acute kidney injury (RIAKI) constitutes roughly 15% of AKI cases, yet its underlying pathophysiology remains poorly understood. Using a murine model of RIAKI induced by muscular glycerol injection, we observed elevated levels of AGEs and the AGE receptor galectin-3 (LGALS3) in the kidney. Immunofluorescence localized LGALS3 to distal nephron segments. According to transcriptomic profiling via next-generation sequencing, RIAKI led to profound changes in kidney metabolism, oxidative stress, and inflammation. Cellular stress was evident in both proximal and distal tubules, as shown by kidney injury markers KIM-1 and NGAL. However, only proximal tubules exhibited overt damage and apoptosis, as detected by routine morphology, active Caspase-3, and TUNEL assay, respectively. In vitro, distal convoluted tubule (DCT) cells challenged with AGEs underwent apoptosis, which was markedly enhanced by Lgals3 siRNA treatment. Thus, in RIAKI, the upregulation of LGALS3 may protect the distal nephron from AGE-mediated damage, while proximal tubules lacking LGALS3 stay at risk. Thus, stimulating LGALS3 in the proximal nephron, if achievable, may attenuate RIAKI.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1571-1585"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141748769","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}
Chae Eun Haam, Sooyeon Choi, Seonhee Byeon, Eun Yi Oh, Soo-Kyoung Choi, Young-Ho Lee
{"title":"Alteration of Piezo1 signaling in type 2 diabetic mice: focus on endothelium and BK<sub>Ca</sub> channel.","authors":"Chae Eun Haam, Sooyeon Choi, Seonhee Byeon, Eun Yi Oh, Soo-Kyoung Choi, Young-Ho Lee","doi":"10.1007/s00424-024-02983-4","DOIUrl":"10.1007/s00424-024-02983-4","url":null,"abstract":"<p><p>Piezo1 mechanosensitive ion channel plays a important role in vascular physiology and disease. This study aimed to elucidate the altered signaling elicited by Piezo1 activation in the arteries of type 2 diabetes. Ten- to 12-week-old male C57BL/6 (control) and type 2 diabetic mice (db<sup>-</sup>/db<sup>-</sup>) were used. The second-order mesenteric arteries (~ 150 μm) were used for isometric tension experiments. Western blot analysis and immunofluorescence staining were performed to observe protein expression. Piezo1 was significantly decreased in mesenteric arteries of type 2 diabetic mice compared to control mice, as analyzed by western blot and immunofluorescence staining. Piezo1 agonist, Yoda1, concentration-dependently induced relaxation of mesenteric arteries in both groups. Interestingly, the relaxation response was significantly greater in control mice than in db<sup>-</sup>/db<sup>-</sup> mice. The removal of endothelium reduced relaxation responses induced by Yoda1, which was greater in control mice than db<sup>-</sup>/db<sup>-</sup> mice. Furthermore, the relaxation response was reduced by pre-treatment with various types of K<sup>+</sup> channel blockers in endothelium-intact arteries in control mice. In endothelium-denuded arteries, pre-incubation with charybdotoxin, an Ca<sup>2+</sup>-activated K<sup>+</sup> channel (BK<sub>Ca</sub> channel) blocker, significantly attenuated Yoda1-induced relaxation in db<sup>-</sup>/db<sup>-</sup> mice, while there was no effect in control mice. Co-immunofluorescence staining showed co-localization of Piezo1 and BK<sub>Ca</sub> channel was more pronounced in db<sup>-</sup>/db<sup>-</sup> mice than in control mice. These results indicate that the vascular responses induced by Piezo1 activation are different in the mesenteric resistance arteries in type 2 diabetic mice.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1479-1492"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492978","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}
Chiara Pappalettera, Silvia Angela Mansi, Marco Arnesano, Fabrizio Vecchio
{"title":"Decoding influences of indoor temperature and light on neural activity: entropy analysis of electroencephalographic signals.","authors":"Chiara Pappalettera, Silvia Angela Mansi, Marco Arnesano, Fabrizio Vecchio","doi":"10.1007/s00424-024-02988-z","DOIUrl":"10.1007/s00424-024-02988-z","url":null,"abstract":"<p><p>Understanding the neural responses to indoor characteristics like temperature and light is crucial for comprehending how the physical environment influences the human brain. Our study introduces an innovative approach using entropy analysis, specifically, approximate entropy (ApEn), applied to electroencephalographic (EEG) signals to investigate neural responses to temperature and light variations in indoor environments. By strategically placing electrodes over specific brain regions linked to temperature and light processing, we show how ApEn can be influenced by indoor factors. We also integrate heart indices from a multi-sensor bracelet to create a machine learning classifier for temperature conditions. Results showed that in anterior frontal and temporoparietal areas, neutral temperature conditions yield higher ApEn values. The anterior frontal area showed a trend of gradually decreasing ApEn values from neutral to warm conditions, with cold being in an intermediate position. There was a significant interaction between light and site factors, only evident in the temporoparietal region. Here, the neutral light condition had higher ApEn values compared to blue and red light conditions. Positive correlations between anterior frontal ApEn and thermal comfort scores suggest a link between entropy and perceived thermal comfort. Our quadratic SVM classifier, incorporating entropy and heart features, demonstrates strong performance (until 90% in terms of AUC, accuracy, sensitivity, and specificity) in classifying temperature sensations. This study offers insights into neural responses to indoor factors and presents a novel approach for temperature classification using EEG entropy and heart features.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":" ","pages":"1539-1554"},"PeriodicalIF":4.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141620680","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}