Biomechanical micromotion at the neural interface modulates intracellular membrane potentials in vivo

Author(s):  
Jonathan Duncan ◽  
Arati Sridharan ◽  
Swathy Sampath Kumar ◽  
Diane Iradukunda ◽  
Jit Muthuswamy
2020 ◽  
Vol 118 (3) ◽  
pp. 290a
Author(s):  
Jonathan L. Duncan ◽  
Swathy Sampath Kumar ◽  
Diane Iradukunda ◽  
Arati Sridharan ◽  
Jitendran Muthuswamy

1980 ◽  
Vol 238 (2) ◽  
pp. H144-H152
Author(s):  
W. J. Stekiel ◽  
W. J. Willems ◽  
D. R. Harder ◽  
J. H. Lombard

To clarify mechanisms leading to failure of compensatory vascular tone in splanchnic blood vessels during prolonged hypotensive stress, anesthetized rats were maintained at a constant mean arterial pressure of 35 mmHg by hemorrhage into an external reservoir until 40% autoinfusion of maximum bled volume. In vivo intracellular membrane potentials (Em) of small intestinal mesenteric veins (300--500 micrometers) were measured before and during the compensatory (bleedout) and decompensatory (autinfusion) phases of the hypotensive period to assess the state of vascular smooth muscle (VSM) excitation. During the compensatory phase, Em decreased from -41 +/- 1 mV (prehemorrhage) to -31 +/- 2 mV, and small venous pressures decreased significantly. The onset of cardiovascular decompensation was associated with hyperpolarization (-53 +/- 3 mV), vasodilation, and return of venous pressure to control levels. Although direct electrical stimulation of the VSM and norepinephrine suffusion still produced constriction late in the hypotensive period, venoconstrictor responses to perivascular nerve stimulation failed progressively. This study indicates that failure of adrenergic neuromuscular transmission contributes significantly to the loss of compensatory VSM tone during hemorrhage.


2012 ◽  
Vol 108 (10) ◽  
pp. 2837-2845 ◽  
Author(s):  
Go Ashida ◽  
Kazuo Funabiki ◽  
Paula T. Kuokkanen ◽  
Richard Kempter ◽  
Catherine E. Carr

Owls use interaural time differences (ITDs) to locate a sound source. They compute ITD in a specialized neural circuit that consists of axonal delay lines from the cochlear nucleus magnocellularis (NM) and coincidence detectors in the nucleus laminaris (NL). Recent physiological recordings have shown that tonal stimuli induce oscillatory membrane potentials in NL neurons (Funabiki K, Ashida G, Konishi M. J Neurosci 31: 15245–15256, 2011). The amplitude of these oscillations varies with ITD and is strongly correlated to the firing rate. The oscillation, termed the sound analog potential, has the same frequency as the stimulus tone and is presumed to originate from phase-locked synaptic inputs from NM fibers. To investigate how these oscillatory membrane potentials are generated, we applied recently developed signal-to-noise ratio (SNR) analysis techniques (Kuokkanen PT, Wagner H, Ashida G, Carr CE, Kempter R. J Neurophysiol 104: 2274–2290, 2010) to the intracellular waveforms obtained in vivo. Our theoretical prediction of the band-limited SNRs agreed with experimental data for mid- to high-frequency (>2 kHz) NL neurons. For low-frequency (≤2 kHz) NL neurons, however, measured SNRs were lower than theoretical predictions. These results suggest that the number of independent NM fibers converging onto each NL neuron and/or the population-averaged degree of phase-locking of the NM fibers could be significantly smaller in the low-frequency NL region than estimated for higher best-frequency NL.


2014 ◽  
Vol 205 (3) ◽  
pp. 377-393 ◽  
Author(s):  
Stéphane Vassilopoulos ◽  
Christel Gentil ◽  
Jeanne Lainé ◽  
Pierre-Olivier Buclez ◽  
Agathe Franck ◽  
...  

The ubiquitous clathrin heavy chain (CHC), the main component of clathrin-coated vesicles, is well characterized for its role in intracellular membrane traffic and endocytosis from the plasma membrane (PM). Here, we demonstrate that in skeletal muscle CHC regulates the formation and maintenance of PM–sarcomere attachment sites also known as costameres. We show that clathrin forms large coated lattices associated with actin filaments and the muscle-specific isoform of α-actinin at the PM of differentiated myotubes. Depletion of CHC in myotubes induced a loss of actin and α-actinin sarcomeric organization, whereas CHC depletion in vivo induced a loss of contractile force due to the detachment of sarcomeres from the PM. Our results suggest that CHC contributes to the formation and maintenance of the contractile apparatus through interactions with costameric proteins and highlight an unconventional role for CHC in skeletal muscle that may be relevant to pathophysiology of neuromuscular disorders.


1985 ◽  
Vol 249 (1) ◽  
pp. C78-C83 ◽  
Author(s):  
H. J. Bryant ◽  
D. R. Harder ◽  
M. B. Pamnani ◽  
F. J. Haddy

Membrane potentials measured in vivo may differ significantly from those measured in vitro in part due to humoral factors, innervation, and wall tension. These studies were initiated to determine whether it is feasible to record membrane potentials from vascular smooth muscle cells in vivo in the caudal artery of the pentobarbital-anesthetized male Wistar rat. Membrane potentials were measured using glass microelectrodes and correlated with systolic, diastolic, and mean blood pressures. For systolic blood pressures between 100 and 140 mmHg the average resting membrane potential was -38.4 +/- 0.48 mV. There was good correlation of systolic, diastolic, and mean blood pressures with membrane potential between 100 and 140 mmHg (r = 0.89, 0.75, and 0.89, respectively). Below 80 mmHg the arterial muscle cells became more depolarized than would be expected if the membrane potential were determined solely by transmural pressure. The depolarized membrane potential at low arterial pressures may be due to enhanced neural input. Spontaneous electrical activity was observed in some of the in vivo cells. When action potentials were present, they were generated at rates between 1-2/s and 6-7/min. These studies indicate that it is feasible to measure membrane potentials from arterial smooth muscle cells in vivo in the caudal artery of the rat.


1996 ◽  
Vol 82 (1) ◽  
pp. 12-21 ◽  
Author(s):  
Lorenzo Maffioli ◽  
Jeroen Steens ◽  
Ernest Pauwels ◽  
Emilio Bombardieri

Hexakis (2-methoxyisobutylisonitrile) technetium-99m (99mTc-SestaMIBI) is a radiopharmaceutical used in nuclear medicine for myocardial perfusion imaging. In the literature different non-cardiac applications of 99mTc-SestaMIBI have been reported. Clinical studies have been performed also in non-oncologic diseases (such as thyroid adenoma, diabetic foot, osteomyelitis, pulmonary actinomycosis, aneurysmal bone cyst, Sudeck's atrophy). Several models for the uptake mechanism of this radiopharmaceutical have been proposed such as binding to an 8-10 kDa cytosolic protein, simple lipid partitioning, or a membrane translocation mechanism involving diffusion and passive transmembrane distribution. Most evidence points in the direction of the third hypothesis. Many studies have indicated that uptake of hexakis (alkylisonitrile) technetium complexes is dependent on mitochondrial and plasma membrane potentials like other lipophilic cations. This explains the initial biodistribution of 99mTc-SestaMIBI to tissues with negative plasma membrane potentials and with a relatively high mitochondrial content (like heart, liver, kidney and skeletal muscle tissue). Malignant tumours also possess these properties in order to maintain their increased metabolism. This behaviour encouraged the study of 99mTc-SestaMIBI as an interesting tracer imaging various tumour types: osteosarcoma, brain, lung, breast, nasopharyngeal, parathyroid, and thyroid cancer. Recent research on cell cellular physiology has further revealed an active transport of 99mTc-SestaMIBI out of the tumour cells, against the potential gradient. The same mechanism is also responsible for resistance to a structurally and functionally different group of cytotoxic agents, such as vinca alkaloids, epipodophyllotoxins, anthracyclins and actinomycin D. This peculiar type of resistance is due to amplification of the mammalian MDR1 gene, located on chromosome 7. For this reason the 99mTc- SestaMIBI uptake in vivo could permit the prediction of the response to the chemotherapy, when the decreased accumulation of 99mTc-SestaMlBI implies the presence of P-gp enriched tissues. In the next future a particular attention should be dedicated to this matter since one of the most important goals of the clinical trials is the demonstration of the usefulness of 99mTc-SestaMIBI for in vivo assessment of multidrug resistance.


Author(s):  
Kanae Hiyoshi ◽  
Narumi Fukuda ◽  
Asuka Shiraishi ◽  
Sachiko Tsuda

2009 ◽  
Vol 4 (3) ◽  
pp. 343-350 ◽  
Author(s):  
Vilma Kisnierienė ◽  
Vidmantas Sakalauskas ◽  
Aleksandras Pleskačiauskas ◽  
Vladimir Yurin ◽  
Osvaldas Rukšėnas

AbstractInterrelations between the action of acetylcholine (ACh) and cadmium ions (Cd2+) on bioelectrogenesis of Nitellopsis obtusa cells were investigated. We analyzed repetitively triggered action potentials (AP), their reproducibility, shape and dynamics of membrane potential after AP induction. ACh significantly increased membrane permeability only at high concentrations (1 mM and 5 mM). Repolarisation level of action potential after the first stimulus was much more positive in all cells treated with ACh as compared to the control. Differences of membrane potentials between points just before the first and the second stimuli were 23.4±.0 mV (control); 40.4±5.9 mV (1 mM ACh solution) and 57.7 ± 8.5 mV (5 mM ACh solution). Cd2+ at 20 μM concentration was examined as a possible inhibitor of acetylcholinesterase (AChE) in vivo. We found that cadmium strengthens depolarizing effect of acetylcholine after the first stimulus. The highest velocity of AP repolarization was reduced after ACh application and Cd2+strengthened this effect. There were no differences in dynamics of membrane potential after repetitively triggered action potentials in ACh or ACh and Cd2+ solutions. This shows that cadmium in small concentration acts as inhibitor of acetylcholinesterase.


2003 ◽  
Vol 773 ◽  
Author(s):  
David J. Edell

AbstractDevelopments in the field of BioMEMS share many of the same issues encountered in the development of neural interface technology that has been underway for many decades. In addition to issues of function, other issues such as biocompatibility and bioresistance have also presented great challenges. The focus of this paper is on the development and testing of electrically insulating biomaterials for micro-devices that can be implanted in biological systems. A variety of accelerated degradation and accelerated detection of degradation techniques have been developed and are used to screen candidate materials. Direct tests of mechanical properties, adhesion, and chemical resistance are used for further assessment. Promising materials indicate what chemistry might be suitable for development of a Chemical Vapor Deposited (CVD) thin film coating. CVD coatings are under development that may be useful for insulation of very small, micromachined elements of an implantable device while only increasing the size of the device by a few micrometers. Materials passing in-vitro testing are then considered for in-vivo testing. Novel instrumentation for testing devices in-vivo has been developed.


Sign in / Sign up

Export Citation Format

Share Document