Membrane potential—Dependent ion channels in cell membrane: Phylogenetic and developmental approaches

Neuroscience ◽  
1984 ◽  
Vol 12 (3) ◽  
pp. 999
Author(s):  
R.D. Vaughan-Jones
Keyword(s):  
Membrane Potential ◽  
Ion Channels ◽  
Cell Membrane

scholarly journals Biophysics and Modeling of Mechanotransduction in Neurons: A Review

Mathematics ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 323
Author(s):  
Martina Nicoletti ◽  
Letizia Chiodo ◽  
Alessandro Loppini
Keyword(s):  
Ion Channels ◽  
Cell Membrane ◽  
Sensory Neurons ◽  
Neuronal Cell ◽  
Molecular Processes ◽  
Biological Mechanisms ◽  
Mechanosensitive Ion Channels ◽  
Complex Interactions ◽  
Different Types ◽  
Intracellular Organelles

Mechanosensing is a key feature through which organisms can receive inputs from the environment and convert them into specific functional and behavioral outputs. Mechanosensation occurs in many cells and tissues, regulating a plethora of molecular processes based on the distribution of forces and stresses both at the cell membrane and at the intracellular organelles levels, through complex interactions between cells’ microstructures, cytoskeleton, and extracellular matrix. Although several primary and secondary mechanisms have been shown to contribute to mechanosensation, a fundamental pathway in simple organisms and mammals involves the presence of specialized sensory neurons and the presence of different types of mechanosensitive ion channels on the neuronal cell membrane. In this contribution, we present a review of the main ion channels which have been proven to be significantly involved in mechanotransduction in neurons. Further, we discuss recent studies focused on the biological mechanisms and modeling of mechanosensitive ion channels’ gating, and on mechanotransduction modeling at different scales and levels of details.

scholarly journals Imaging the transmembrane and transendothelial sodium gradients in gliomas

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Muhammad H. Khan ◽  
John J. Walsh ◽  
Jelena M. Mihailović ◽  
Sandeep K. Mishra ◽  
Daniel Coman ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Magnetic Resonance ◽  
Cell Membrane ◽  
Normal Tissue ◽  
Magnetic Resonance Spectroscopic Imaging ◽  
Biological Factors ◽  
High Sodium ◽  
Intracellular Milieu

AbstractUnder normal conditions, high sodium (Na+) in extracellular (Na+e) and blood (Na+b) compartments and low Na+ in intracellular milieu (Na+i) produce strong transmembrane (ΔNa+mem) and weak transendothelial (ΔNa+end) gradients respectively, and these manifest the cell membrane potential (Vm) as well as blood–brain barrier (BBB) integrity. We developed a sodium (23Na) magnetic resonance spectroscopic imaging (MRSI) method using an intravenously-administered paramagnetic polyanionic agent to measure ΔNa+mem and ΔNa+end. In vitro 23Na-MRSI established that the 23Na signal is intensely shifted by the agent compared to other biological factors (e.g., pH and temperature). In vivo 23Na-MRSI showed Na+i remained unshifted and Na+b was more shifted than Na+e, and these together revealed weakened ΔNa+mem and enhanced ΔNa+end in rat gliomas (vs. normal tissue). Compared to normal tissue, RG2 and U87 tumors maintained weakened ΔNa+mem (i.e., depolarized Vm) implying an aggressive state for proliferation, whereas RG2 tumors displayed elevated ∆Na+end suggesting altered BBB integrity. We anticipate that 23Na-MRSI will allow biomedical explorations of perturbed Na+ homeostasis in vivo.

Pressure-induced smooth muscle cell depolarization in pulmonary arteries from control and chronically hypoxic rats does not cause myogenic vasoconstriction

2005 ◽  
Vol 98 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
Jay S. Naik ◽  
Scott Earley ◽  
Thomas C. Resta ◽  
Benjimen R. Walker
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arteries ◽  
Barometric Pressure ◽  
Cell Membrane Potential ◽  
Intraluminal Pressure ◽  
Dose Dependent

Chronic obstructive pulmonary diseases, as well as prolonged residence at high altitude, can result in generalized airway hypoxia, eliciting an increase in pulmonary vascular resistance. We hypothesized that a portion of the elevated pulmonary vascular resistance following chronic hypoxia (CH) is due to the development of myogenic tone. Isolated, pressurized small pulmonary arteries from control (barometric pressure ≅ 630 Torr) and CH (4 wk, barometric pressure = 380 Torr) rats were loaded with fura 2-AM and perfused with warm (37°C), aerated (21% O2-6% CO2-balance N2) physiological saline solution. Vascular smooth muscle (VSM) intracellular Ca2+ concentration ([Ca2+]i) and diameter responses to increasing intraluminal pressure were determined. Diameter and VSM cell [Ca2+]i responses to KCl were also determined. In a separate set of experiments, VSM cell membrane potential responses to increasing luminal pressure were determined in arteries from control and CH rats. VSM cell membrane potential in arteries from CH animals was depolarized relative to control at each pressure step. VSM cells from both groups exhibited a further depolarization in response to step increases in intraluminal pressure. However, arteries from both control and CH rats distended passively to increasing intraluminal pressure, and VSM cell [Ca2+]i was not affected. KCl elicited a dose-dependent vasoconstriction that was nearly identical between control and CH groups. Whereas KCl administration resulted in a dose-dependent increase in VSM cell [Ca2+]i in arteries taken from control animals, this stimulus elicited only a slight increase in VSM cell [Ca2+]i in arteries from CH animals. We conclude that the pulmonary circulation of the rat does not demonstrate pressure-induced vasoconstriction.

Pancreatic beta-cell electrical activity: the role of anions and the control of pH

1983 ◽  
Vol 244 (3) ◽  
pp. C188-C197 ◽  
Author(s):  
G. T. Eddlestone ◽  
P. M. Beigelman
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Proton Exchange ◽  
Disulfonic Acid ◽  
Control Mechanisms ◽  
Exchange System ◽  
Sodium Proton Exchange

The influence of chloride on the mouse pancreatic beta-cell membrane potential and the cell membrane mechanisms controlling intracellular pH (pHi) have been investigated using glass microelectrodes to monitor the membrane potential. It has been shown that chloride is distributed passively across the beta-cell membrane such that chloride potential is equal to the membrane potential. Withdrawal of perifusate chloride or bicarbonate and the application of the drugs 4-acetamido-4'-isethiocyanostilbene-2,2'-disulfonic acid (SITS) and probenecid, both blockers of transmembrane anion movement, have been used to establish that a chloride-bicarbonate exchange system is operative in the cell membrane and that it is one of the control mechanisms of pHi. Amiloride, a specific blocker of the transmembrane sodium proton exchange, has been used to demonstrate that this mechanism is also operative in the beta-cell membrane in the control of pHi. The hypothesis that the calcium-activated potassium permeability is proton sensitive at an intracellular site, a fall in pHi causing a fall in permeability and an increase in pHi causing an increase in permeability, has been used to explain many of the effects observed in this study.

The stimulant action of acetylcholine and catecholamines on the uterus

1973 ◽  
Vol 265 (867) ◽  
pp. 149-156 ◽  
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Membrane Conductance ◽  
Primary Effect ◽  
Force Of Contraction ◽  
Chloride Permeability ◽  
Duration Of Action ◽  
Spike Discharge ◽  
Calcium Permeability

The α action of catecholamines on oestrogen dominated guinea-pig uterus is stimulant. The cell membrane is depolarized, membrane conductance is increased, spike discharge is accelerated and tension develops. This action resembles that of acetylcholine though catecholamines are less potent, and, in equiactive concentrations, catecholamines have a longer latency and a longer duration of action. Evidence, obtained by modifications of the ionic environment, indicates that the depolarization by acetylcholine is due to an increase in sodium and calcium permeability and that acetylcholine can release calcium from intracellular stores. The depolarization by catecholamines is due to an increase in chloride permeability and, in addition, sodium is required for the ensuing increase of spike discharge. Catecholamines produce an increase in the force of contraction, long outlasting their immediate stimulation. Moreover, their effect on membrane potential and membrane conductance persists in the presence of lanthanum. These results suggest that Ca release from intracellular stores may be the primary effect produced by the α action of catecholamines and that the increase in the cytoplasmic Ca 2+ concentration may cause the changes at the cell membrane.

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