scholarly journals Thermal Mechanisms of Millimeter Wave Stimulation of Excitable Cells

2013 ◽  
Vol 104 (12) ◽  
pp. 2622-2628 ◽  
Author(s):  
Mikhail G. Shapiro ◽  
Michael F. Priest ◽  
Peter H. Siegel ◽  
Francisco Bezanilla
Keyword(s):  
Millimeter Wave ◽  
Excitable Cells ◽  
Stimulation Of

scholarly journals Calmidazolium and arachidonate activate a calcium entry pathway that is distinct from store-operated calcium influx in HeLa cells

2004 ◽  
Vol 381 (3) ◽  
pp. 929-939 ◽  
Author(s):  
Claire M. PEPPIATT ◽  
Anthony M. HOLMES ◽  
Jeong T. SEO ◽  
Martin D. BOOTMAN ◽  
Tony J. COLLINS ◽  
...  
Keyword(s):  
Hela Cells ◽  
Calcium Influx ◽  
Differential Sensitivity ◽  
Excitable Cells ◽  
Hormonal Stimulation ◽  
Calmodulin Antagonist ◽  
Alternative Pathways ◽  
Entry Pathway ◽  
Store Depletion ◽  
Stimulation Of

Agonists that deplete intracellular Ca2+ stores also activate Ca2+ entry, although the mechanism by which store release and Ca2+ influx are linked is unclear. A potential mechanism involves ‘store-operated channels’ that respond to depletion of the intracellular Ca2+ pool. Although SOCE (store-operated Ca2+ entry) has been considered to be the principal route for Ca2+ entry during hormonal stimulation of non-electrically excitable cells, recent evidence has suggested that alternative pathways activated by metabolites such as arachidonic acid are responsible for physiological Ca2+ influx. It is not clear whether such messenger-activated pathways exist in all cells, whether they are truly distinct from SOCE and which metabolites are involved. In the present study, we demonstrate that HeLa cells express two pharmacologically and mechanistically distinct Ca2+ entry pathways. One is the ubiquitous SOCE route and the other is an arachidonate-sensitive non-SOCE. We show that both these Ca2+ entry pathways can provide long-lasting Ca2+ elevations, but that the channels are not the same, based on their differential sensitivity to 2-aminoethoxydiphenyl borate, LOE-908 {(R,S)-(3,4-dihydro-6,7-dimethoxy-isochinolin-1-yl)-2-phenyl-N,N-di[2-(2,3,4-trimethoxyphenyl)ethyl]acetamid mesylate} and gadolinium. In addition, non-SOCE and not SOCE was permeable to strontium. Furthermore, unlike SOCE, the non-SOCE pathway did not require store depletion and was not sensitive to displacement of the endoplasmic reticulum from the plasma membrane using jasplakinolide or ionomycin pretreatment. These pathways did not conduct Ca2+ simultaneously due to the dominant effect of arachidonate, which rapidly curtails SOCE and promotes Ca2+ influx via non-SOCE. Although non-SOCE could be activated by exogenous application of arachidonate, the most robust method for stimulation of this pathway was application of the widely used calmodulin antagonist calmidazolium, due to its ability to activate phospholipase A2.

scholarly journals Modeling the role of endoplasmic reticulum-mitochondria microdomains in calcium dynamics

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Arash Moshkforoush ◽  
Baarbod Ashenagar ◽  
Nikolaos M. Tsoukias ◽  
B. Rita Alevriadou
Keyword(s):  
Endoplasmic Reticulum ◽  
Vascular Endothelial Cells ◽  
Cell Model ◽  
Vascular Endothelial ◽  
Calcium Dynamics ◽  
Mitochondrial Membranes ◽  
Excitable Cells ◽  
Closed Cell ◽  
Stimulation Of

AbstractUpon inositol trisphosphate (IP3) stimulation of non-excitable cells, including vascular endothelial cells, calcium (Ca2+) shuttling between the endoplasmic reticulum (ER) and mitochondria, facilitated by complexes called Mitochondria-Associated ER Membranes (MAMs), is known to play an important role in the occurrence of cytosolic Ca2+ concentration ([Ca2+]Cyt) oscillations. A mathematical compartmental closed-cell model of Ca2+ dynamics was developed that accounts for ER-mitochondria Ca2+ microdomains as the µd compartment (besides the cytosol, ER and mitochondria), Ca2+ influx to/efflux from each compartment and Ca2+ buffering. Varying the distribution of functional receptors in MAMs vs. the rest of ER/mitochondrial membranes, a parameter called the channel connectivity coefficient (to the µd), allowed for generation of [Ca2+]Cytoscillations driven by distinct mechanisms at various levels of IP3 stimulation. Oscillations could be initiated by the transient opening of IP3 receptors facing either the cytosol or the µd, and subsequent refilling of the respective compartment by Ca2+ efflux from the ER and/or the mitochondria. Only under conditions where the µd became the oscillation-driving compartment, silencing the Mitochondrial Ca2+ Uniporter led to oscillation inhibition. Thus, the model predicts that alternative mechanisms can yield [Ca2+]Cyt oscillations in non-excitable cells, and, under certain conditions, the ER-mitochondria µd can play a regulatory role.

Sound localization in anurans. I. Evidence of binaural interaction in dorsal medullary nucleus of bullfrogs (Rana catesbeiana)

1976 ◽  
Vol 39 (4) ◽  
pp. 871-881 ◽  
Author(s):  
A. S. Feng ◽  
R. R. Capranica
Keyword(s):  
Rana Catesbeiana ◽  
Single Cells ◽  
Tone Burst ◽  
Excitatory Input ◽  
The Other ◽  
Excitable Cells ◽  
Tuning Curves ◽  
Contralateral Ear ◽  
Dorsal Medullary Nucleus ◽  
Stimulation Of

1. The response patterns of single cells to monaural and binaural acoustic stimuli were studied in the dorsal medullary nucleus of the bullfrog (Rana catesbeiana). This nucleus represents the first ascending center in the anuran's central auditory nervous system. 2. Of the 142 cells isolated, 75 units responded only to monaural stimulation. Approximately 80% of these monaural cells could be excited by the ipsilateral ear, while the remaining 20% received their excitatory input from the contralateral ear. The other 67 units responded to binaural stimuli. Of these binaural cells, 14 could be excited by either contralateral or ipsilateral stimuli, and the threshold and best excitatory frequency were similar for each ear (EE). The other 53 binaural cells (EI) could be excited by stimulation of one ear and inhibited by stimulation of the other ear; for almost all of these cells the contralateral ear was excitatory and the ipsilateral ear was inhibitory. The best inhibitory frequency for one ear was approximately the same as the best excitatory frequency for the other ear, and the threshold for inhibition was near the threshold for excitation. 3. The tuning curves for all of the cells in the dorsal medullary nucleus were unimodal with "Q" values ranging from 0.4 to 4. The excitatory thresholds were widely scattered between 22 and 115 dB SPL. 4. The distribution of best excitatory frequencies for the monaural cells comprised three groups: 200-300, 500-800, and 900-1,600 Hz. The best excitatory frequencies of the binaural cells were scattered over this entire range, with a broad peak around 200-800 Hz. 5. Approximately 80% of the cells in the dorsal nucleus responded tonically throughout the duration of an excitatory tone burst. The remaining 20% of the cells responded phasically during the transient stages of a tone burst over a wide intensity range. 6. Response latencies were compared for the two types of monaural cells to tones at their best exciatatory frequencies at 10 dB above threshold. The latencies for the contralaterally excitable cells were just a few milliseconds longer than the latencies for the ipsilaterally excitable cells. For binaural cells the latency for contralateral stimulation was only 1-2 ms longer than for ipsilateral stimulation. It was concluded that the contralateral input to the dorsal medullary nucleus is not of efferent descending origin from higher auditory centers. 7. All of the binaural EI cells were sensitive to small interaural intensity differences and many were also sensitive to minute interaural time differences.These cells likely play a role in localization of sounds of significance to anurans.

Review on Electromagnetic Stimulation of Alive Tissues

2016 ◽  
Vol 0 (0) ◽  
Author(s):  
Oana Drosu ◽  
Marilena Stanculescu
Keyword(s):  
Magnetic Field ◽  
Chemical Transport ◽  
Biological Tissues ◽  
The Body ◽  
Excitable Cells ◽  
Electromagnetic Stimulation ◽  
Excitable Tissue ◽  
First Case ◽  
The Magnetic Field ◽  
Stimulation Of

AbstractThe electric, magnetic or electromagnetic phenomena that occur in the biological tissues include: the behavior of excitable tissue (the sources), the electric currents and potentials in the volume conductor, the magnetic field at and beyond the body, the response of excitable cells to electric and magnetic field stimulation (through changes in their electrical activity, changes of chemical transport through cell membrane); the intrinsic electric and magnetic properties of the tissue. This paper presents an overview of fundamental phenomena occurring in the application of stimuli with a future purpose of focusing on several models of external electromagnetic stimulation. The target is to create models of the electroconductive anatomy of some alive tissues will be proposed, in order to investigate the fields and the currents generated by the on-set of an electric field (in the first case) or a time-variant magnetic field (in the second case) or the superposition of the two types of stimuli.

scholarly journals Ca2+ entry into PC12 cells initiated by ryanodine receptors or inositol 1,4,5-trisphosphate receptors

1998 ◽  
Vol 329 (2) ◽  
pp. 349-357 ◽  
Author(s):  
L. Deborah BENNETT ◽  
D. Martin BOOTMAN ◽  
J. Michael BERRIDGE ◽  
R. Timothy CHEEK
Keyword(s):  
Endoplasmic Reticulum ◽  
Pc12 Cells ◽  
Ryanodine Receptors ◽  
Half Time ◽  
Free Medium ◽  
Excitable Cells ◽  
Inositol 1,4,5 Trisphosphate ◽  
Insp3 Receptors ◽  
Universal Mechanism ◽  
Stimulation Of

Capacitative Ca2+ entry (CCE) is a universal mechanism for refilling intracellular Ca2+ stores in electrically non-excitable cells. The situation in excitable cells is less clear, however, since they may rely on other entry mechanisms for Ca2+-store refilling. In the present study we investigated CCE in intact PC12 cells, using acetylcholine to bring about activation of InsP3 receptors (InsP3Rs), caffeine to activate ryanodine receptors (RyRs) and thapsigargin to inhibit sarco/endoplasmic reticulum Ca2+-ATPase pumps. We found that depletion of the InsP3-, caffeine- or thapsigargin-sensitive stores promoted Ca2+ entry, suggesting that stimulation of either InsP3Rs or RyRs can activate CCE. The CCE pathways activated by InsP3Rs, RyRs and thapsigargin appeared to be independent at least in part, since their effects were found to be additive. However, CCE triggered by caffeine, acetylcholine or thapsigargin progressively diminished with time. The decay of CCE caused by one agent also inhibited subsequent responses to the others, suggesting that some component of the CCE pathway is common to all intracellular Ca2+ stores. The magnitude of CCE stimulated by InsP3Rs or RyRs was related to the size of the stores; the InsP3-sensitive store was smaller than the RyR-sensitive store and triggered a smaller entry component. However, both stores filled with a similar half time (about 1 min), and both could be filled more rapidly by depolarization-induced Ca2+ entry through voltage-operated channels. A significant basal Ca2+ influx was apparent in PC12 cells. The basal entry component may be under the control of the InsP3-sensitive Ca2+ store, since short incubations in Ca2+-free medium depleted this store.

scholarly journals Effective Ultrasonic Stimulation in Human Peripheral Nervous System

2021 ◽  
Author(s):  
Thomas Riis ◽  
Jan Kubanek
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Low Frequency ◽  
Controlled Study ◽  
Excitable Cells ◽  
Low Frequencies ◽  
Ultrasound Frequency ◽  
Nociceptive Responses ◽  
Ultrasonic Stimulation ◽  
Stimulation Of

AbstractObjectiveLow-intensity ultrasound can stimulate excitable cells in a noninvasive and targeted manner, but which parameters are effective has remained elusive. This question has been difficult to answer because differences in transducers and parameters—frequency in particular—lead to profound differences in the stimulated tissue volumes. The objective of this study is to control for these differences and evaluate which ultrasound parameters are effective in stimulating excitable cells.MethodsHere, we stimulated the human peripheral nervous system using a single transducer operating in a range of frequencies, and matched the stimulated volumes with an acoustic aperture.ResultsWe found that low frequencies (300 kHz) are substantially more effective in generating tactile and nociceptive responses in humans compared to high frequencies (900 kHz). The strong effect of ultrasound frequency was observed for all pressures tested, for continuous and pulsed stimuli, and for tactile and nociceptive responses.ConclusionThis prominent effect may be explained by a mechanical force associated with ultrasound. The effect is not due to heating, which would be weaker at the low frequency.SignificanceThis controlled study reveals that ultrasonic stimulation of excitable cells is stronger at lower frequencies, which guides the choice of transducer hardware for effective ultrasonic stimulation of the peripheral nervous system in humans.

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