3 Microelectrode Techniques: Equipment, Components, and Systems

2004 ◽  
Keyword(s):  
Microelectrode Techniques

Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells

1998 ◽  
Vol 274 (3) ◽  
pp. H829-H845 ◽  
Author(s):  
Bum-Rak Choi ◽  
Guy Salama
Keyword(s):  
Action Potentials ◽  
Imaging Techniques ◽  
Atrioventricular Node ◽  
Small Cells ◽  
Av Node ◽  
Propagation Pattern ◽  
Voltage Sensitive Dyes ◽  
Decremental Conduction ◽  
Microelectrode Techniques ◽  
Av Delay

The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the “compact” node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks I and III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II) represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Acetylcholine lengthens action potentials of sheep cardiac Purkinje fibers

1980 ◽  
Vol 238 (2) ◽  
pp. H237-H243
Author(s):  
S. L. Lipsius ◽  
W. R. Gibbons
Keyword(s):  
Muscarinic Receptors ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Purkinje Fibers ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
Rate Of Increase ◽  
Definite Sequence ◽  
Microelectrode Techniques ◽  
Diastolic Potential

The effect of acetylcholine (ACh) on the electrical activity of sheep cardiac Purkinje fibers was studied using standard microelectrode techniques. Most fibers showed a definite sequence of changes when exposed to ACh. Initially, action potential duration (APD) increased markedly. After about 20 s, the maximum diastolic potential (MDP) started to become more negative and, at the same time, the rate of increase in APD slowed. Once the MDP stabilized at a more negative level, the APD usually resumed its rapid increase. ACh also increased the slope of diastolic depolarization and made the plateau voltage more positive. APD was increased by ACh concentrations as low as 10(-7) M, and it increased with concentrations up to 10(-5) M (the highest concentration tested). ACh-induced increases in APD depended on the stimulation frequency; 2-min exposures to 10(-6) M ACh increased APD by 76.8 +/- 14.7% at 6 min-1 and 17.7 +/- 4.2% at 60 min-1. Atropine blocked all the effects of ACh. Hexamethonium did not prevent the ACh effects. It is concluded that ACh acts via muscarinic receptors. The changes in APD and MDP appear to be separate events, and it is difficult to see how the former effect may be explained by known actions of ACh.

Persistence of the electrophysiologic effects of mexiletine in canine Purkinje fibers alters the response to subsequent hypoxia

1987 ◽  
Vol 65 (10) ◽  
pp. 2104-2109
Author(s):  
Neil D. Berman ◽  
Richard I. Ogilvie ◽  
James E. Loukides
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Free Solution ◽  
Purkinje Fibers ◽  
Subsequent Exposure ◽  
Hydrochloride Solution ◽  
Drug Free ◽  
Microelectrode Techniques ◽  
Upstroke Velocity ◽  
Normal Formula

The persistence of cellular electropharmacologic effects of mexiletine on canine Purkinje fibers was studied utilizing standard microelectrode techniques and two different protocols. In the first, the tissue was exposed to hypoxic perfusion before and 30 min after perfusion with one of the following: mexiletine hydrochloride 6.25 μM solution, mexiletine hydrochloride 12.5 μM solution, or drug-free Tyrode's solution. With the higher concentration of mexiletine, depression of the maximal upstroke velocity [Formula: see text] persisted 30 min after drug washout and subsequent exposure to hypoxia did not result in the anticipated shortening of action potential duration but did prevent the restoration of normal [Formula: see text]. After perfusion with the lower concentration of mexiletine, [Formula: see text] was not depressed and hypoxic action potential duration shortening was not prevented. In the second protocol, Purkinje fibers were perfused with 12.5 μM mexiletine hydrochloride solution and then exposed to hypoxia after 15, 30,45, or 60 min of perfusion with drug-free solution. Depression of maximal upstroke velocity and shortening of action potential duration persisted during washout, returning to control values by 45 min, although mexiletine was not detectable in the tissue bath after 10 min of washout. Hypoxia initiated at 15 or 30 min of washout failed to produce the anticipated shortening of action potential duration. At 45 and 60 min, action potential duration was shortened by hypoxia. We concluded that mexiletine depression of [Formula: see text] and shortening of action potential duration may persist in the absence of drug. Further shortening of action potential duration in response to hypoxia is prevented during this period. The persistence of [Formula: see text] depression is prolonged by hypoxia.

Microelectrode studies of the tegument and sub-tegumental compartments of male Schistosoma mansoni: an analysis of electrophysiological properties

Parasitology ◽  
1982 ◽  
Vol 85 (1) ◽  
pp. 163-178 ◽  
Author(s):  
D. P. Thompson ◽  
R. A. Pax ◽  
J. L. Bennett
Keyword(s):  
Schistosoma Mansoni ◽  
Electrical Potential ◽  
Input Resistance ◽  
Time Constants ◽  
Current Spreading ◽  
Electrophysiological Properties ◽  
Length Constant ◽  
Zero Potential ◽  
Microelectrode Techniques ◽  
Multiple Electrode

SUMMARYStandard intracellular microelectrode techniques were used to determine the electrical properties of the tegument and sub-tegumental regions in male Schistosoma mansoni. Three distinct compartments of electrical potential were observed. The resting potentials recorded in these compartments of –45·9±2·5 mV (Eteg), –22·0±1·1 mV (E2) and – 4·7±0·3 mV (E3) corroborate those previously reported by Fetterer, Pax & Bennett (1980) and Bricker, Pax & Bennett (1981). Input resistance was measured in each compartment and was found to be 4·5 MΩ (tegument), 9·2 MΩ (E2) and 3·5 MΩ (E3). Time-constants for the tegument, E2 and E3 were 0·24±0·01 msec, 0·25±0·01 msec and 0·13±0·01 msec, respectively. Multiple electrode experiments revealed that the tegument and E2 compartment are electrical syncytia with similar current-spreading capabilities. Low resistance pathways also appear to connect the tegument and E2 region, since electrotonic signals initiated in either of those compartments experience only a 15–25% reduction upon passing into the other. Injecting large (> 200 nA) depolarizing current pulses into the tegument or E2 compartment often resulted in the initiation of active membrane responses. These spikes were highly variable, ranging from 4 to 75 mV in magnitude (occasionally overshooting zero potential by as much as 25 mV) and from 10–40 msec in duration. The responses were not actively propagated along the parasite, and their decay over distance was approximately equal to that predicted on the basis of length constant values obtained from electrotonic signals. The addition of a non-diffusible solute to the recording medium resulted in a significant reduction in the current-spreading capacity of both the tegument and E2 compartment. Coupling ratios between the tegument and E2 compartment were decreased, and the input resistance for both compartments increased, while resting potentials remained constant. Active responses could not be evoked in schistosomes exposed to the hyperosmotic medium.

Letters to the Editor

1998 ◽  
Vol 275 (5) ◽  
pp. H1905-H1909 ◽  
Author(s):  
Igor R. Efimov
Keyword(s):  
Imaging Techniques ◽  
Atrioventricular Node ◽  
Small Cells ◽  
Letters To The Editor ◽  
Av Node ◽  
Propagation Pattern ◽  
Voltage Sensitive Dyes ◽  
Decremental Conduction ◽  
Microelectrode Techniques ◽  
Av Delay

The following is an abstract of the article discussed in the subsequent letter:  Choi, Bum-Rak, and Guy Salama. Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells. Am. J. Physiol. 274 ( Heart Circ. Physiol. 43): H829–H845, 1998.—The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the “compact” node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks Iand III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II)represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Respiratory Au nucleation and microelectrode techniques reveal key features of bacterial conductive matrix

2020 ◽  
Vol 7 (10) ◽  
pp. 3189-3200
Author(s):  
María Victoria Ordóñez ◽  
Luciana Robuschi ◽  
Cristina Elena Hoppe ◽  
Juan Pablo Busalmen
Keyword(s):  
Gold Nanoparticles ◽  
Electron Transfer ◽  
Transfer Mechanism ◽  
Extracellular Electron Transfer ◽  
Electron Transfer Mechanism ◽  
Key Features ◽  
Microelectrode Techniques

Key elements of Geobacter's extracellular electron transfer mechanism are characterized combining respiratory formed gold nanoparticles with spectro-electrochemical and microelectrode techniques.

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