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.

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.

Postnatal Development of Electrophysiological Properties of Nucleus Accumbens Neurons

2000 ◽  
Vol 84 (5) ◽  
pp. 2204-2216 ◽  
Author(s):  
Marc L. Belleau ◽  
Richard A. Warren
Keyword(s):  
Nucleus Accumbens ◽  
Postnatal Development ◽  
Action Potentials ◽  
Membrane Resistance ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Projection Neurons ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Wide Range

We have studied the postnatal development of the physiological characteristics of nucleus accumbens (nAcb) neurons in slices from postnatal day 1 ( P1) to P49 rats using the whole cell patch-clamp technique. The majority of neurons (102/108) were physiologically identified as medium spiny (MS) projection neurons, and only these were subjected to detailed analysis. The remaining neurons displayed characteristics suggesting that they were not MS neurons. Around the time of birth and during the first postnatal weeks, the membrane and firing characteristics of MS neurons were quite different from those observed later. These characteristics changed rapidly during the first 3 postnatal weeks, at which point they began to resemble those found in adults. Both whole cell membrane resistance and membrane time constant decreased more than fourfold during the period studied. The resting membrane potential (RMP) also changed significantly from an average of −50 mV around birth to less than −80 mV by the end of the third postnatal week. During the first postnatal week, the current-voltage relationship of all encountered MS neurons was linear over a wide range of membrane potentials above and below RMP. Through the second postnatal week, the proportion of neurons displaying inward rectification in the hyperpolarized range increased steadily and after P15, all recorded MS neurons displayed significant inward rectification. At all ages, inward rectification was blocked by extracellular cesium and tetra-ethyl ammonium and was not changed by 4-aminopyridine; this shows that inward rectification was mediated by the same currents in young and mature MS neurons. MS neurons fired single and repetitive Na+/K+ action potentials as early as P1. Spike threshold and amplitude remained constant throughout development in contrast to spike duration, which decreased significantly over the same period. Depolarizing current pulses from rest showed that immature MS neurons fired action potentials more easily than their older counterparts. Taken together, the results from the present study suggest that young and adult nAcb MS neurons integrate excitatory synaptic inputs differently because of differences in their membrane and firing properties. These findings provide important insights into signal processing within nAcb during this critical period of development.

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.

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.

Potassium distribution and membrane potential of sensory neurons in the leech nervous system

1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Sensory Neurons ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Bathing Medium ◽  
Membrane Hyperpolarization ◽  
K Concentration ◽  
Intracellular K Activity ◽  
K Activity

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)

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.

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.

Cyclic nucleotides in spinal cells

1976 ◽  
Vol 54 (3) ◽  
pp. 416-421 ◽  
Author(s):  
K. Krnjevic ◽  
W. G. Van Meter
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Cyclic Nucleotides ◽  
Membrane Resistance ◽  
Resting Membrane Potential ◽  
Cyclic Monophosphate ◽  
Synaptic Facilitation ◽  
Marked Enhancement

The most striking effects of intracellular injections of adenosine 3′5′-cyclic monophosphate (cAMP) into spinal mononeurons in cats are a speeding-up of the action potential, both its rising and falling phase, and a potentiation of the after-hyperpolarization; the latter probably indicates a marked enhancement of Ca2+ influx. In this respect, cAMP and guanosine 3′5′-cyclic monophosphate (cGMP) have similar actions, though cAMP appears to be more potent. It is suggested that through this mechanism, cyclic nucleotides may play an important role in synaptic facilitation. Changes in resting membrane potential and resistance are less conspicuous or predictable. By contrast, both agents, when injected into unresponsive cells, presumed to be neuroglia, regularly cause a drop in membrane resistance; this is associated with hyperpolarization and therefore likely to reflect an increase in membrane K+ conductance.

Depression of glutamate-mediated synaptic transmission by benzyl alcohol

1977 ◽  
Vol 55 (4) ◽  
pp. 917-922 ◽  
Author(s):  
Carol A. Colton ◽  
Joel S. Colton
Keyword(s):  
Membrane Potential ◽  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Benzyl Alcohol ◽  
Reversal Potential ◽  
Membrane Resistance ◽  
Postsynaptic Membrane ◽  
Resting Membrane Potential ◽  
End Plate ◽  
Potential Frequency

The data obtained from this study suggest that the nonionizable anesthetic benzyl alcohol has two prominent actions on GABA- and glutamate-mediated synaptic transmission at the lobster neuromuscular junction. They are as follows: (1) depression of the excitatory end-plate potential and the postsynaptic membrane response to applied glutamate, and (2) a hyperpolarization of the postsynaptic resting membrane potential associated with a decrease in effective membrane resistance. No change in amplitude of the inhibitory end-plate potential or inhibitory reversal potential was seen. Excitatory miniature end-plate potential frequency was also unaffected. The depression of excitatory synaptic transmission appears to be due to a decreased responsiveness of the postsynaptic receptor–ionophore complex.

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