Distance-Dependent Modifiable Threshold for Action Potential Back-Propagation in Hippocampal Dendrites

2003 ◽  
Vol 90 (3) ◽  
pp. 1807-1816 ◽  
Author(s):  
C. Bernard ◽  
D. Johnston
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Opposite Effect ◽  
Pyramidal Neurons ◽  
Back Propagation ◽  
Dendritic Tree ◽  
Resting Membrane Potential ◽  
Hippocampal Ca1 ◽  
Dendritic Location ◽  
Partial Blockade

In hippocampal CA1 pyramidal neurons, action potentials generated in the axon back-propagate in a decremental fashion into the dendritic tree where they affect synaptic integration and synaptic plasticity. The amplitude of back-propagating action potentials (b-APs) is controlled by various biological factors, including membrane potential ( Vm). We report that, at any dendritic location ( x), the transition from weak (small-amplitude b-APs) to strong (large-amplitude b-APs) back-propagation occurs when Vm crosses a threshold potential, θ x. When Vm > θ x, back-propagation is strong (mostly active). Conversely, when Vm < θ x, back-propagation is weak (mostly passive). θ x varies linearly with the distance ( x) from the soma. Close to the soma, θ x ≪ resting membrane potential (RMP) and a strong hyperpolarization of the membrane is necessary to switch back-propagation from strong to weak. In the distal dendrites, θ x ≫ RMP and a strong depolarization is necessary to switch back-propagation from weak to strong. At ∼260 μm from the soma, θ260 ≈ RMP, suggesting that in this dendritic region back-propagation starts to switch from strong to weak. θ x depends on the availability or state of Na+ and K+ channels. Partial blockade or phosphorylation of K+ channels decreases θ x and thereby increases the portion of the dendritic tree experiencing strong back-propagation. Partial blockade or inactivation of Na+ channels has the opposite effect. We conclude that θ x is a parameter that captures the onset of the transition from weak to strong back-propagation. Its modification may alter dendritic function under physiological and pathological conditions by changing how far large action potentials back-propagate in the dendritic tree.

The generation of electric currents in cardiac fibers by Na/Ca exchange

1979 ◽  
Vol 236 (3) ◽  
pp. C103-C110 ◽  
Author(s):  
L. J. Mullins
Keyword(s):  
Membrane Potential ◽  
Duty Cycle ◽  
Action Potentials ◽  
Reversal Potential ◽  
Resting Membrane Potential ◽  
Electrochemical Gradient ◽  
Ca Current ◽  
Cardiac Action ◽  
Cardiac Fiber ◽  
Cardiac Fibers

The presence of a detectable Ca current during the excitation of a cardiac fiber implies that the Ca lost during the resting interval of the duty cycle must also be detectable. Ca outward movement appears to be effected by Na/Ca exchange when more Na enters than Ca leaves per cycle, thus making the mechanism electrogenic. Since Na/Ca exchange can move Ca either inward or outward depending on the direction of the electrochemical gradient for Na, a potential exists where there is no electric current generated by the Na/Ca exchange mechanism, i.e., a reversal potential ER. Cardiac fibers appear to have a reversal potential that is about midway between their resting membrane potential and their plateau. Carrier currents both inward and outward are therefore generated during cardiac action potentials. The implications of the conditions stated above are explored.

scholarly journals Membrane Dysfunction Induced by In Vitro Ischemia in Rat Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 81 (4) ◽  
pp. 1872-1880 ◽  
Author(s):  
E. Tanaka ◽  
S. Yamamoto ◽  
H. Inokuchi ◽  
T. Isagai ◽  
H. Higashi
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Pyramidal Neurons ◽  
Membrane Surface ◽  
Bathing Medium ◽  
Ca1 Pyramidal Neurons ◽  
In Vitro Ischemia ◽  
Hippocampal Ca1 ◽  
Electrode Voltage

Membrane dysfunction induced by in vitro ischemia in rat hippocampal CA1 pyramidal neurons. Intracellular and single-electrode voltage-clamp recordings were made to investigate the process of membrane dysfunction induced by superfusion with oxygen and glucose-deprived (ischemia-simulating) medium in hippocampal CA1 pyramidal neurons of rat tissue slices. To assess correlation between potential change and membrane dysfunction, the recorded neurons were stained intracellularly with biocytin. A rapid depolarization was produced ∼6 min after starting superfusion with ischemia-simulating medium. When oxygen and glucose were reintroduced to the bathing medium immediately after generating the rapid depolarization, the membrane did not repolarize but depolarized further, the potential reaching 0 mV ∼5 min after the reintroduction. In single-electrode voltage-clamp recording, a corresponding rapid inward current was observed when the membrane potential was held at −70 mV. After the reintroduction of oxygen and glucose, the current induced by ischemia-simulating medium partially returned to preexposure levels. These results suggest that the membrane depolarization is involved with the membrane dysfunction. The morphological aspects of biocytin-stained neurons during ischemic exposure were not significantly different from control neurons before the rapid depolarization. On the other hand, small blebs were observed on the surface of the neuron within 0.5 min of generating the rapid depolarization, and blebs increased in size after 1 min. After 3 min, neurons became larger and swollen. The long and transverse axes and area of the cross-sectional cell body were increased significantly 1 and 3 min after the rapid depolarization. When Ca2+-free (0 mM) with Co2+ (2.5 mM)-containing medium including oxygen and glucose was applied within 1 min after the rapid depolarization, the membrane potential was restored completely to the preexposure level in the majority of neurons. In these neurons, the long axis was lengthened without any blebs being apparent on the membrane surface. These results suggest that the membrane dysfunction induced by in vitro ischemia may be due to a Ca2+-dependent process that commences ∼1.5 min after and is completed 3 min after the onset of the rapid depolarization. Because small blebs occurred immediately after the rapid depolarization and large blebs appeared 1.5–3 min after, it is likely that the transformation from small to large blebs may result in the observed irreversible membrane dysfunction.

Membrane Properties Underlying Patterns of GABA-Dependent Action Potentials in Developing Mouse Hypothalamic Neurons

2001 ◽  
Vol 86 (3) ◽  
pp. 1252-1265 ◽  
Author(s):  
Yu-Feng Wang ◽  
Xiao-Bing Gao ◽  
Anthony N. van den Pol
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Brain Slices ◽  
Reversal Potential ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Hypothalamic Neurons ◽  
Spike Threshold ◽  
Spike Patterns

Spikes may play an important role in modulating a number of aspects of brain development. In early hypothalamic development, GABA can either evoke action potentials, or it can shunt other excitatory activity. In both slices and cultures of the mouse hypothalamus, we observed a heterogeneity of spike patterns and frequency in response to GABA. To examine the mechanisms underlying patterns and frequency of GABA-evoked spikes, we used conventional whole cell and gramicidin perforation recordings of neurons ( n = 282) in slices and cultures of developing mouse hypothalamus. Recorded with gramicidin pipettes, GABA application evoked action potentials in hypothalamic neurons in brain slices of postnatal day 2–9( P2- 9) mice. With conventional patch pipettes (containing 29 mM Cl−), action potentials were also elicited by GABA from neurons of 2–13 days in vitro (2–13 DIV) embryonic hypothalamic cultures. Depolarizing responses to GABA could be generally classified into three types: depolarization with no spike, a single spike, or complex patterns of multiple spikes. In parallel experiments in slices, electrical stimulation of GABAergic mediobasal hypothalamic neurons in the presence of glutamate receptor antagonists [10 μM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 100 μM 2-amino-5-phosphonopentanoic acid (AP5)] resulted in the occurrence of spikes that were blocked by bicuculline (20 μM). Blocking ionotropic glutamate receptors with AP5 and CNQX did not block GABA-mediated multiple spikes. Similarly, when synaptic transmission was blocked with Cd2+ (200 μM) and Ni2+(300 μM), GABA still induced multiple spikes, suggesting that the multiple spikes can be an intrinsic membrane property of GABA excitation and were not based on local interneurons. When the pipette [Cl−] was 29 or 45 mM, GABA evoked multiple spikes. In contrast, spikes were not detected with 2 or 10 mM intracellular [Cl−]. With gramicidin pipettes, we found that the mean reversal potential of GABA-evoked current ( E GABA) was positive to the resting membrane potential, suggesting a high intracellular [Cl−] in developing mouse neurons. Varying the holding potential from −80 to 0 mV revealed an inverted U-shaped effect on spike probability. Blocking voltage-dependent Na+ channels with tetrodotoxin eliminated GABA-evoked spikes, but not the GABA-evoked depolarization. Removing Ca2+ from the extracellular solution did not block spikes, indicating GABA-evoked Na+-based spikes. Although E GABA was more positive within 2–5 days in culture, the probability of GABA-evoked spikes was greater in 6- to 9-day cells. Mechanistically, this appears to be due to a greater Na+ current found in the older cells during a period when the E GABA is still positive to the resting membrane potential. GABA evoked similar spike patterns in HEPES and bicarbonate buffers, suggesting that Cl−, not bicarbonate, was primarily responsible for generatingmultiple spikes. GABA evoked either single or multiple spikes; neurons with multiple spikes had a greater Na+ current, a lower conductance, a more negative spike threshold, and a greater difference between the peak of depolarization and the spike threshold. Taken together, the present results indicate that the patterns of multiple action potentials evoked by GABA are an inherent property of the developing hypothalamic neuron.

scholarly journals The Effect of Aconitine on the Giant Axon of the Squid

1964 ◽  
Vol 47 (4) ◽  
pp. 719-733 ◽  
Author(s):  
W. H. Herzog ◽  
R. M. Feibel ◽  
S. H. Bryant
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Giant Axon ◽  
Membrane Resistance ◽  
Repetitive Stimulation ◽  
Resting Membrane Potential ◽  
Sustained Activity ◽  
Frequency Of Stimulation ◽  
Sodium And Potassium

In the giant axon of Loligo pealii, "aconitine potent" Merck added to the bath (10-7 to 1.25 x 10-6 gm/ml) (a) had no effect on resting membrane potential, membrane resistance and rectification, membrane response to subthreshold currents, critical depolarization, or action potential, but (b) on repetitive stimulation produced oscillations of membrane potential after the spike, depolarization, and decrease of membrane resistance. The effect sums with successive action potentials; it increases with concentration of aconitine, time of exposure, and frequency of stimulation. When the oscillations are large enough and the membrane potential is 51.6 ± SD 1.5 mv a burst of self-sustained activity begins; it usually lasts 20 to 70 sec. and at its end the membrane potential is 41.5 ± SD 1.9 mv. Repolarization occurs with a time constant of 2.5 to 11.1 min. Substitution of choline for external sodium after a burst hyperpolarizes the membrane to -70 mv, and return to normal external sodium depolarizes again beyond the resting membrane potential. The effect of aconitine on the membrane is attributed to an increase of sodium and potassium or chloride conductances following the action potential.

Electrophysiological observations on diaphragm muscle from normal and dystrophic hamsters

1985 ◽  
Vol 63 (11) ◽  
pp. 1474-1476 ◽  
Author(s):  
E. G. Hunter ◽  
J. Elbrink
Keyword(s):  
Membrane Potential ◽  
Electrical Activity ◽  
Action Potentials ◽  
Membrane Potentials ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Rapid Decline ◽  
Action Potential Amplitude ◽  
Dystrophic Muscle ◽  
Adenosine Triphosphate Production

The cellular electrical activity of diaphragm from F1B normal and BIO 14.6 dystrophic hamsters has been investigated using microelectrodes. Resting membrane potentials and action potentials were recorded from control muscles and from muscles exposed to 2,4-dinitrophenol. The action potentials of normal and dystrophic diaphragms were similar in amplitude and configuration. Treatment with 2,4-dinitrophenol caused the action potential amplitude of both diaphragms to decline by similar amounts. The control resting membrane potential of diaphragm from dystrophic hamsters is not significantly different from that of normal hamsters. Treatment with 2,4-dinitrophenol caused a linear decrease in the resting membrane potentials of both groups of muscles. Dystrophic muscle, however, showed a more rapid decline in excitability when exposed to 2,4-dinitrophenol. This suggests that adenosine triphosphate production in dystrophic muscle is partially inhibited as has been suggested by other workers.

scholarly journals Electrophysiology of the Heart of an Isopod Crustacean: Porcellio Dilatatus

1972 ◽  
Vol 57 (3) ◽  
pp. 609-631
Author(s):  
J. C. DELALEU ◽  
A. BLONDEAU ◽  
A. HOLLEY
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Additional Data ◽  
Ionic Currents ◽  
Membrane Resistance ◽  
Resting Membrane Potential ◽  
Plateau Phase ◽  
Bathing Medium ◽  
Ionic Conductances ◽  
Rate Of Decline

1. The effects of various ions and chemicals were tested on the resting or active membrane of the heart of the wood-louse Porcellio dilatatus. 2. The curve relating the resting membrane potential to log [K+]o was found to correspond with the theoretical curve expected from the Nernst equation at higher concentrations only. Excess K+ decreased both amplitude and rate of rise of the response while the rate of decline was increased. In K+-deficient solutions the duration of the plateau phase was at first increased, then depressed. The addition of K+ to a bathing medium deprived for several minutes of this ion caused a large increase in the membrane potential and in the response height. The way in which the membrane was seen to react was tentatively attributed to an electrogenic active pumping mechanism. 3. In Na+-deficient solutions, the rate of rise and the height of the response were reduced while the resting membrane potential was decreased. 4. Ca2+-deficient solutions depolarized the membrane and decreased both amplitude and duration of the response. Cessation of activity occurred in Ca2+-free solution. In excess calcium the membrane was hyperpolarized. The rhythm and the rate of rising were decreased and the plateau phase depressed. 5. TTX blocked the heart activity, probably by acting upon the heart ganglion. Mn2+ depressed especially the humped plateau (when present) of the spontaneous responses. 6. TEA, caffeine and procaine transformed spontaneous activity of weak amplitude into large and complex overshooting responses. In TEA solutions, several stable levels of polarization were observed. Contrary to what occurred in the normal solution, depolarizing current pulses could trigger large all-or-none action potentials when TEA was present. 7. The TEA-induced regenerative response was analysed with the help of an intracellular stimulating current when [Na+]o and [Ca2+]o were varied. Additional data were obtained by applying TTX, Mn2+ or GABA. From the results, both Ca2+ and Na+ were thought to be involved in the ionic currents underlying spike type activity. 8. The spike-generating effect of TEA has been attributed to its property of increasing the membrane resistance and of allowing the ionic conductances which generate the weakly active component of the normal response, the plateau, but not the initial upstroke, to be amplified regeneratively. 9. The large spikes elicited by TEA were found relatively less effective than weak sustained depolarization in inducing strong contractions. 10. The functional significance of the data was tentatively interpreted by comparison with the properties of the heart of Limulus, Crustacea and vertebrates.

Ratiometry of transmembrane voltage-sensitive fluorescent dye emission in hearts

2000 ◽  
Vol 279 (3) ◽  
pp. H1421-H1433 ◽  
Author(s):  
Stephen B. Knisley ◽  
Robert K. Justice ◽  
Wei Kong ◽  
Philip L. Johnson
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Signal To Noise Ratio ◽  
Green Emission ◽  
Motion Artifacts ◽  
Resting Membrane Potential ◽  
Baseline Drift ◽  
Fluorescence Measurements ◽  
Transmembrane Voltage ◽  
Voltage Dependent

Transmembrane voltage-sensitive fluorescence measurements are limited by baseline drift that can obscure changes in resting membrane potential and by motion artifacts that can obscure repolarization. Voltage-dependent shift of emission wavelengths may allow reduction of drift and motion artifacts by emission ratiometry. We have tested this for action potentials and potassium-induced changes in resting membrane potential in rabbit hearts stained with di-4-ANEPPS [Pyridinium, 4-(2-(6-(dibutylamino)-2-naphthalenyl) ethenyl)-1-(3-sulfopropyl)-, hydroxide, inner salt] using laser excitation (488 nm) and a two-photomultiplier tube system or spectrofluorometer (resolution of 500–1,000 Hz and <1 mm). Green and red emissions produced upright and inverted action potentials, respectively. Ratios of green emission to red emission followed action potential contours and exhibited larger fractional changes than either emission alone ( P < 0.001). The largest changes and signal-to-noise ratio (signal/noise) were obtained with numerator wavelengths of 525–550 nm and denominator wavelengths of 650–700 nm. Ratiometry lessened drift 56–66% ( P < 0.015) and indicated decreases in resting membrane potential. Ratiometry lessened motion artifacts and increased magnitudes of deflections representing phase-zero depolarizations relative to total deflections by 123–188% in intact hearts ( P < 0.02). Durations of action potentials at different pacing rates, temperatures, and potassium concentrations were independent of whether they were measured ratiometrically or with microelectrodes ( P ≥ 0.65). The ratiometric calibration slope was 0.017/100 mV and decreased with time. Thus emission ratiometry lessens the effects of motion and drift and indicates resting membrane potential changes and repolarization.

Sodium dependence of the thyrotrophin-induced depolarization in cultured porcine thyroid cells

1986 ◽  
Vol 108 (2) ◽  
pp. 225-230 ◽  
Author(s):  
T. A. Hambleton ◽  
J. R. Bourke ◽  
G. J. Huxham ◽  
S. W. Manley
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Potassium Concentration ◽  
Sodium Current ◽  
Resting Membrane Potential ◽  
Thyroid Cell ◽  
Free Medium ◽  
Thyroid Cells ◽  
Voltage Dependent ◽  
Sodium And Potassium

ABSTRACT Cultured porcine thyroid cells exhibit a resting membrane potential of about − 73 mV and depolarize to about − 54 mV on exposure to TSH. The depolarizing response to TSH was preserved in a medium consisting only of inorganic salts and buffers, but was abolished in sodium-free medium, demonstrating dependence on an inward sodium current. Increasing the potassium concentration of the medium resulted in a reduction in the resting membrane potential of 60 mV per tenfold change in potassium concentration, and a diminished TSH response. A hyperpolarizing TSH response was observed in a sodium- and bicarbonate-free medium, indicating that a hyperpolarizing ion current (probably carried by potassium) was also enhanced in the presence of TSH. Tetrodotoxin blocked the TSH response. We conclude that the response of the thyroid cell membrane to TSH involves increases in permeability to sodium and potassium, and that the thyroid membrane ion channels bear some similarity to the voltage-dependent sodium channels of excitable tissues, despite the absence of action potentials in the thyroid. J. Endocr. (1986) 108, 225–230

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