Neuroethological Role of Dynamic Traits of Excitable Cells: A Proposal for the Physiological Basis of Slothfulness in the Sloth

1983 ◽  
pp. 535-544
Author(s):  
Theodore Holmes Bullock
Keyword(s):  
Excitable Cells ◽  
Physiological Basis ◽  
Dynamic Traits

Physiological basis of feeding behavior inTritonia diomedea. III. Role of depolarizing afterpotentials

1981 ◽  
Vol 12 (5) ◽  
pp. 515-532 ◽  
Author(s):  
Andrew G. M. Bulloch ◽  
A. O. Dennis Willows
Keyword(s):  
Feeding Behavior ◽  
Physiological Basis

scholarly journals Calnexin revealed as an ether-a-go-go chaperone by getting mutant worms up and going

2018 ◽  
Vol 150 (8) ◽  
pp. 1059-1061
Author(s):  
Jonathan T. Pierce
Keyword(s):  
Ion Channels ◽  
Dynamic Control ◽  
Cell Types ◽  
K Channel ◽  
Membrane Domains ◽  
Excitable Cells ◽  
Patch Clamp Recording ◽  
Cell Excitability ◽  
Distinct Membrane

The role of ion channels in cell excitability was first revealed in a series of voltage clamp experiments by Hodgkin and Huxley in the 1950s. However, it was not until the 1970s that patch-clamp recording ushered in a revolution that allowed physiologists to witness how ion channels flicker open and closed at angstrom scale and with microsecond resolution. The unexpectedly tight seal made by the patch pipette in the whole-cell configuration later allowed molecular biologists to suck up the insides of identified cells to unveil their unique molecular contents. By refining these techniques, researchers have scrutinized the surface and contents of excitable cells in detail over the past few decades. However, these powerful approaches do not discern which molecules are responsible for the dynamic control of the genesis, abundance, and subcellular localization of ion channels. In this dark territory, teams of unknown and poorly understood molecules guide specific ion channels through translation, folding, and modification, and then they shuttle them toward and away from distinct membrane domains via different subcellular routes. A central challenge in understanding these processes is the likelihood that these diverse regulatory molecules may be specific to ion channel subtypes, cell types, and circumstance. In work described in this issue, Bai et al. (2018. J. Gen. Physiol. https://doi.org/10.1085/jgp.201812025) begin to shed light on the biogenesis of UNC-103, a K+ channel found in Caenorhabditis elegans.

Role of Cyclic Nucleotides in Excitable Cells

1980 ◽  
Vol 42 (1) ◽  
pp. 629-641 ◽  
Author(s):  
I Kupfermann
Keyword(s):  
Cyclic Nucleotides ◽  
Excitable Cells

PHYSICAL ACTIVITY AS HEALTHY INTERVENTION AGAINST SEVERE OXIDATIVE STRESS IN ELDERLY POPULATION

2013 ◽  
pp. 1-9
Author(s):  
C. TOMAS-ZAPICO ◽  
E. IGLESIAS-GUTIERREZ ◽  
B. FERNANDEZ-GARCIA ◽  
D. DE GONZALO-CALVO
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Elderly Population ◽  
Physiological Basis ◽  
Related Disease ◽  
Age Related ◽  
Wide Range ◽  
Health Related ◽  
Relevant Risk Factor

Severe oxidative stress is a relevant risk factor for major deleterious health-related events in olderpeople and is thought to be an important contributor to age-related disease. Literature has suggested oxidativestress as a therapeutic target for mitigating the biological decline and attenuating the occurrence of adverseclinical events in aged individuals. However, definitive treatments are not known. Regular and moderate physicalactivity has been proposed as possible intervention for slowing age-related decline. This healthy strategy presentsa wide range of beneficial aspects for elderly, from the reduction of morbidity, disability, frailty and mortalityrates to treatment of many age-related disorders. Importantly, the global benefits on health are not shared by anyother strategies. Nevertheless, the physiological basis by which exercise produces its benefits to the organism isnot fully understood. This review summarizes the evidence for the role of physical activity as potential healthyintervention for mitigating the negative aspects of aging through the modulation of the oxidative mechanisms.

scholarly journals Essential Role of Hemoglobin βCys93 in Cardiovascular Physiology

Physiology ◽  
2020 ◽  
Vol 35 (4) ◽  
pp. 234-243 ◽  
Author(s):  
Richard T. Premont ◽  
Jonathan S. Stamler
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Tissue Hypoxia ◽  
Microvascular Blood Flow ◽  
Cardiovascular Physiology ◽  
Transient Ischemia ◽  
Microcirculatory Blood Flow ◽  
Physiological Basis ◽  
Hb S

The supply of oxygen to tissues is controlled by microcirculatory blood flow. One of the more surprising discoveries in cardiovascular physiology is the critical dependence of microcirculatory blood flow on a single conserved cysteine within the β-subunit (βCys93) of hemoglobin (Hb). βCys93 is the primary site of Hb S-nitrosylation [i.e., S-nitrosothiol (SNO) formation to produce S-nitrosohemoglobin (SNO-Hb)]. Notably, S-nitrosylation of βCys93 by NO is favored in the oxygenated conformation of Hb, and deoxygenated Hb releases SNO from βCys93. Since SNOs are vasodilatory, this mechanism provides a physiological basis for how tissue hypoxia increases microcirculatory blood flow (hypoxic autoregulation of blood flow). Mice expressing βCys93A mutant Hb (C93A) have been applied to understand the role of βCys93, and RBCs more generally, in cardiovascular physiology. Notably, C93A mice are unable to effect hypoxic autoregulation of blood flow and exhibit widespread tissue hypoxia. Moreover, reactive hyperemia (augmentation of blood flow following transient ischemia) is markedly impaired. C93A mice display multiple compensations to preserve RBC vasodilation and overcome tissue hypoxia, including shifting SNOs to other thiols on adult and fetal Hbs and elsewhere in RBCs, and growing new blood vessels. However, compensatory vasodilation in C93A mice is uncoupled from hypoxic control, both peripherally (e.g., predisposing to ischemic injury) and centrally (e.g., impairing hypoxic drive to breathe). Altogether, physiological studies utilizing C93A mice are confirming the allosterically controlled role of SNO-Hb in microvascular blood flow, uncovering essential roles for RBC-mediated vasodilation in cardiovascular physiology and revealing new roles for RBCs in cardiovascular disease.

Mineral Cycling and Lichens: The Physiological Basis

1991 ◽  
Vol 23 (3) ◽  
pp. 293-307 ◽  
Author(s):  
Dennis H. Brown ◽  
Rosalie M. Brown
Keyword(s):  
Toxic Metal ◽  
Distribution Patterns ◽  
Essential Elements ◽  
Mineral Matter ◽  
Physiological Basis ◽  
Wet And Dry Deposition ◽  
Mineral Cycling ◽  
Physiological Processes ◽  
Field And Laboratory Conditions

AbstractA number of physiological processes relevant to the role of lichens in mineral cycling are discussed. Consideration is given to the cellular location of positively-charged cations, showing (a) the benefits of quantifying intracellular elements for the interpretation of toxic metal stress, and (b) how distribution patterns of physiologically essential elements may be altered by desiccation and rehydration under field and laboratory conditions. The quantitative significance of these dynamic processes associated with metal uptake and loss requires verification under field conditions. A modified sequential elution procedure is proposed that enables quantification of insoluble paniculate mineral matter (acquired by wet and dry deposition) in addition to soluble elements in intercellular, extracellular-exchangeable and intracellular sites.

scholarly journals Silencing of Plasma Membrane Ca2+-ATPase Isoforms 2 and 3 Impairs Energy Metabolism in Differentiating PC12 Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Tomasz Boczek ◽  
Malwina Lisek ◽  
Bozena Ferenc ◽  
Antoni Kowalski ◽  
Magdalena Wiktorska ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Pc12 Cells ◽  
Molecular Mechanisms ◽  
Atp Synthesis ◽  
Mitochondrial Activity ◽  
Excitable Cells ◽  
Close Link ◽  
Atp Level ◽  
Atp Generation

A close link between Ca2+, ATP level, and neurogenesis is apparent; however, the molecular mechanisms of this relationship have not been completely elucidated. Transient elevations of cytosolic Ca2+may boost ATP synthesis, but ATP is also consumed by ion pumps to maintain a low Ca2+in cytosol. In differentiation process plasma membrane Ca2+ATPase (PMCA) is considered as one of the major players for Ca2+homeostasis. From four PMCA isoforms, the fastest PMCA2 and PMCA3 are expressed predominantly in excitable cells. In the present study we assessed whether PMCA isoform composition may affect energy balance in differentiating PC12 cells. We found that PMCA2-downregulated cells showed higher basal O2consumption, lower NAD(P)H level, and increased activity of ETC. These changes associated with higher[Ca2+]cresulted in elevated ATP level. Since PMCA2-reduced cells demonstrated greatest sensitivity to ETC inhibition, we suppose that the main source of energy for PMCA isoforms 1, 3, and 4 was oxidative phosphorylation. Contrary, cells with unchanged PMCA2 expression exhibited prevalence of glycolysis in ATP generation. Our results with PMCA2- or PMCA3-downregulated lines provide an evidence of a novel role of PMCA isoforms in regulation of bioenergetic pathways, and mitochondrial activity and maintenance of ATP level during PC12 cells differentiation.

scholarly journals Inositol 1,4,5-Trisphosphate Directs Ca2+Flow between Mitochondria and the Endoplasmic/Sarcoplasmic Reticulum: A Role in Regulating Cardiac Autonomic Ca2+ Spiking

2000 ◽  
Vol 11 (5) ◽  
pp. 1845-1858 ◽  
Author(s):  
Marisa Jaconi ◽  
Claire Bony ◽  
Stephen M. Richards ◽  
André Terzic ◽  
Serge Arnaudeau ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Dominant Negative ◽  
Neonatal Rat ◽  
Excitable Cells ◽  
Rat Cardiomyocytes ◽  
Cell Functions ◽  
Inositol 1,4,5 Trisphosphate ◽  
Cellular Ca ◽  
Cardiac Autonomic Activity

The signaling role of the Ca2+ releaser inositol 1,4,5-trisphosphate (IP3) has been associated with diverse cell functions. Yet, the physiological significance of IP3 in tissues that feature a ryanodine-sensitive sarcoplasmic reticulum has remained elusive. IP3 generated by photolysis of caged IP3 or by purinergic activation of phospholipase Cγ slowed down or abolished autonomic Ca2+ spiking in neonatal rat cardiomyocytes. Microinjection of heparin, blocking dominant-negative fusion protein, or anti-phospholipase Cγ antibody prevented the IP3-mediated purinergic effect. IP3 triggered a ryanodine- and caffeine-insensitive Ca2+ release restricted to the perinuclear region. In cells loaded with Rhod2 or expressing a mitochondria-targeted cameleon and TMRM to monitor mitochondrial Ca2+ and potential, IP3 induced transient Ca2+ loading and depolarization of the organelles. These mitochondrial changes were associated with Ca2+ depletion of the sarcoplasmic reticulum and preceded the arrest of cellular Ca2+ spiking. Thus, IP3 acting within a restricted cellular region regulates the dynamic of calcium flow between mitochondria and the endoplasmic/sarcoplasmic reticulum. We have thus uncovered a novel role for IP3 in excitable cells, the regulation of cardiac autonomic activity.

scholarly journals TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications

2017 ◽  
Vol 50 (5) ◽  
pp. 1700754 ◽  
Author(s):  
Andrea Olschewski ◽  
Emma L. Veale ◽  
Bence M. Nagy ◽  
Chandran Nagaraj ◽  
Grazyna Kwapiszewska ◽  
...  
Keyword(s):  
Pulmonary Circulation ◽  
Cell Biology ◽  
Unsaturated Fatty Acids ◽  
Excitable Cells ◽  
Intracellular Signalling Pathways ◽  
Current State ◽  
Health And Disease ◽  
Pulmonary Arterial ◽  
Pore Domain

TWIK-related acid-sensitive potassium channel 1 (TASK-1 encoded by KCNK3) belongs to the family of two-pore domain potassium channels. This gene subfamily is constitutively active at physiological resting membrane potentials in excitable cells, including smooth muscle cells, and has been particularly linked to the human pulmonary circulation. TASK-1 channels are sensitive to a wide array of physiological and pharmacological mediators that affect their activity such as unsaturated fatty acids, extracellular pH, hypoxia, anaesthetics and intracellular signalling pathways. Recent studies show that modulation of TASK-1 channels, either directly or indirectly by targeting their regulatory mechanisms, has the potential to control pulmonary arterial tone in humans. Furthermore, mutations in KCNK3 have been identified as a rare cause of both familial and idiopathic pulmonary arterial hypertension. This review summarises our current state of knowledge of the functional role of TASK-1 channels in the pulmonary circulation in health and disease, with special emphasis on current advancements in the field.

scholarly journals Role of STIM1 protein in the regulation of store-operated channels in non-excitable cells

2009 ◽  
Vol 3 (3) ◽  
pp. 329-329
Author(s):  
I. A. Pozdnjakov ◽  
V. A. Vigont ◽  
O. A. Zimina ◽  
A. Yu. Skopin ◽  
L. N. Glushankova ◽  
...  
Keyword(s):  
Excitable Cells
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