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

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.

1962 ◽  
Vol 45 (6) ◽  
pp. 1195-1216 ◽  
Author(s):  
Fred J. Julian ◽  
John W. Moore ◽  
David E. Goldman

A method similar to the sucrose-gap technique introduced be Stäpfli is described for measuring membrane potential and current in singly lobster giant axons (diameter about 100 micra). The isotonic sucrose solution used to perfuse the gaps raises the external leakage resistance so that the recorded potential is only about 5 per cent less than the actual membrane potential. However, the resting potential of an axon in the sucrose-gap arrangement is increased 20 to 60 mv over that recorded by a conventional micropipette electrode when the entire axon is bathed in sea water. A complete explanation for this effect has not been discovered. The relation between resting potential and external potassium and sodium ion concentrations shows that potassium carries most of the current in a depolarized axon in the sucrose-gap arrangement, but that near the resting potential other ions make significant contributions. Lowering the external chloride concentration decreases the resting potential. Varying the concentration of the sucrose solution has little effect. A study of the impedance changes associated with the action potential shows that the membrane resistance decreases to a minimum at the peak of the spike and returns to near its initial value before repolarization is complete (a normal lobster giant axon action potential does not have an undershoot). Action potentials recorded simultaneously by the sucrose-gap technique and by micropipette electrodes are practically superposable.


1976 ◽  
Vol 54 (3) ◽  
pp. 416-421 ◽  
Author(s):  
K. Krnjevic ◽  
W. G. Van Meter

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.


1957 ◽  
Vol 40 (6) ◽  
pp. 859-885 ◽  
Author(s):  
Ichiji Tasaki ◽  
Susumu Hagiwara

1. Intracellular injection of tetraethylammonium chloride (TEA) into a giant axon of the squid prolongs the duration of the action potential without changing the resting potential (Fig. 3). The prolongation is sometimes 100-fold or more. 2. The action potential of a giant axon treated with TEA has an initial peak followed by a plateau (Fig. 3). The membrane resistance during the plateau is practically normal (Fig. 4). Near the end of the action potential, there is an apparent increase in the membrane resistance (Fig. 5D and Fig. 6, right). 3. The phenomenon of abolition of action potentials was demonstrated in the squid giant axon treated with TEA (Fig. 7). Following an action potential abolished in its early phase, there is no refractoriness (Fig. 8). 4. By the method of voltage clamp, the voltage-current relation was investigated on normal squid axons as well as on axons treated with TEA (Figs. 9 and 10). 5. The presence of stable states of the membrane was demonstrated by clamping the membrane potential with two voltage steps (Fig. 11). Experimental evidence was presented showing that, in an "unstable" state, the membrane conductance is not uniquely determined by the membrane potential. 6. The effect of low sodium water was investigated in the axon treated with TEA (Fig. 12). 7. The similarity between the action potential of a squid axon under TEA and that of the vertebrate cardiac muscle was stressed. The experimental results were interpreted as supporting the view that there are two stable states in the membrane. Initiation and abolition of an action potential were explained as transitions between the two states.


1972 ◽  
Vol 57 (3) ◽  
pp. 609-631
Author(s):  
J. C. DELALEU ◽  
A. BLONDEAU ◽  
A. HOLLEY

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.


1986 ◽  
Vol 108 (2) ◽  
pp. 225-230 ◽  
Author(s):  
T. A. Hambleton ◽  
J. R. Bourke ◽  
G. J. Huxham ◽  
S. W. Manley

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


1976 ◽  
Vol 230 (2) ◽  
pp. 403-409 ◽  
Author(s):  
HK Jacobs ◽  
FE South

Resting and action potential parameters were measured from papillary muscle isolated from hibernating and control hamsters and from rats. The temperature range of the study was 12-38 degrees C. The decrease in resting membrane potential (Em) with decreasing temperature was significantly less in the hibernation preparations (HH), down to 20 degrees C, than in either the control hamsters or rats. Below 20 degrees C the declines in Em of all preparations were indistinguishable. Action potential magnitude was adequately maintained in HH to 12 degrees C while both control hamster and rat action potentials declined markedly as temperatures were reduced. Both types of hamster preparations showed greatly prolonged action potentials with reduced temperatures as contrasted to a limited prolongation of rat action potentials. The data are suggestive of a membrane modication in hibernation.


2004 ◽  
Vol 286 (6) ◽  
pp. C1246-C1257 ◽  
Author(s):  
Kevin S. Thorneloe ◽  
Mark T. Nelson

Urinary bladder smooth muscle (UBSM) elicits depolarizing action potentials, which underlie contractile events of the urinary bladder. The resting membrane potential of UBSM is approximately −40 mV and is critical for action potential generation, with hyperpolarization reducing action potential frequency. We hypothesized that a tonic, depolarizing conductance was present in UBSM, functioning to maintain the membrane potential significantly positive to the equilibrium potential for K+ ( EK; −85 mV) and thereby facilitate action potentials. Under conditions eliminating the contribution of K+ and voltage-dependent Ca2+ channels, and with a clear separation of cation- and Cl−-selective conductances, we identified a novel background conductance ( Icat) in mouse UBSM cells. Icat was mediated predominantly by the influx of Na+, although a small inward Ca2+ current was detectable with Ca2+ as the sole cation in the bathing solution. Extracellular Ca2+, Mg2+, and Gd3+ blocked Icat in a voltage-dependent manner, with Ki values at −40 mV of 115, 133, and 1.3 μM, respectively. Although UBSM Icat is extensively blocked by physiological extracellular Ca2+ and Mg2+, a tonic, depolarizing Icat was detected at −40 mV. In addition, inhibition of Icat demonstrated a hyperpolarization of the UBSM membrane potential and decreased the amplitude of phasic contractions of isolated UBSM strips. We suggest that Icat contributes tonically to the depolarization of the UBSM resting membrane potential, facilitating action potential generation and thereby a maintenance of urinary bladder tone.


The Neuron ◽  
2015 ◽  
pp. 103-126
Author(s):  
Irwin B. Levitan ◽  
Leonard K. Kaczmarek

The flow of ions down their electrochemical gradients, through populations of ion channels in the neuronal plasma membrane, gives rise to transmembrane ion currents. It is the sum of the various currents flowing at any point in time that determines the neuron’s membrane potential. Thus the normal firing pattern of a neuron, and its response to different kinds of stimulation, can be seen as a play of interactions among the currents flowing through the different kinds of ion channels in its membrane. The activities of the sodium and potassium channels responsible for axonal action potentials are themselves dependent on voltage. Voltage clamp studies, which allow the measurement of the current flowing through these channels at fixed voltage, have provided a detailed understanding of the sequence of changes in sodium and potassium channel activity that give rise to action potentials.


1986 ◽  
Vol 251 (4) ◽  
pp. H710-H715
Author(s):  
W. W. Tse

The canine atrioventricular (AV) junction comprises three major tissues: paranodal fibers (PNF), AV node (AVN), and His bundle (HB). In the present study, dissection-exposed, in vitro canine AV junctional preparations were used. The object of the study was to determine whether the PNF or AVN was more sensitive to the suppressive effect of acetylcholine (ACh). In five experiments these tissues were stimulated antegradely and retrogradely, and their action potentials were recorded simultaneously under the influence of ACh (0.5 micrograms/ml). Results indicated the PNF were more sensitive to the suppressive effect of ACh than were the AVN. In another group of 13 experiments, the effects of ACh at 0.05-0.3 micrograms/ml on rate of rise of phase 0 of action potentials (Vmax), peak potential, resting membrane potential, and action potential duration of the PNF were determined. Results indicated that ACh exerted a strong suppressive effect on Vmax and amplitude of the action potentials and had little effect on the resting membrane potential and action potential duration of the PNF. In 10 of 13 preparations, ACh also suppressed the response of PNF, resulting in generation of one action potential to every two stimuli. In conclusion, these findings suggest that PNF could be the tissue responsible for vagal-induced AV conduction block.


2002 ◽  
Vol 88 (4) ◽  
pp. 2058-2074 ◽  
Author(s):  
Arturas Grigaliunas ◽  
Robert M. Bradley ◽  
Donald K. MacCallum ◽  
Charlotte M. Mistretta

Neurons in trigeminal and geniculate ganglia extend neurites that share contiguous target tissue fields in the fungiform papillae and taste buds of the mammalian tongue and thereby have principal roles in lingual somatosensation and gustation. Although functional differentiation of these neurons is central to formation of lingual sensory circuits, there is little known about electrophysiological properties of developing trigeminal and geniculate ganglia or the extrinsic factors that might regulate neural development. We used whole cell recordings from embryonic day 16 rat ganglia, maintained in culture as explants for 3–10 days with neurotrophin support to characterize basic properties of trigeminal and geniculate neurons over time in vitro and in comparison to each other. Each ganglion was cultured with the neurotrophin that supports maximal neuron survival and that would be encountered by growing neurites at highest concentration in target fields. Resting membrane potential and time constant did not alter over days in culture, whereas membrane resistance decreased and capacitance increased in association with small increases in trigeminal and geniculate soma size. Small gradual differences in action potential properties were observed for both ganglion types, including an increase in threshold current to elicit an action potential and a decrease in duration and increase in rise and fall slopes so that action potentials became shorter and sharper with time in culture. Using a period of 5–8 days in culture when neural properties are generally stable, we compared trigeminal and geniculate ganglia and revealed major differences between these embryonic ganglia in passive membrane and action potential characteristics. Geniculate neurons had lower resting membrane potential and higher input resistance and smaller, shorter, and sharper action potentials with lower thresholds than trigeminal neurons. Whereas all trigeminal neurons produced a single action potential at threshold depolarization, 35% of geniculate neurons fired repetitively. Furthermore, all trigeminal neurons produced TTX-resistant action potentials, but geniculate action potentials were abolished in the presence of low concentrations of TTX. Both trigeminal and geniculate neurons had inflections on the falling phase of the action potential that were reduced in the presence of various pharmacological blockers of calcium channel activation. Use of nifedipine, ω-conotoxin-MVIIA and GVIA, and ω-agatoxin-TK indicated that currents through L-, N-, and P/Q- type calcium channels participate in the action potential inflection in embryonic trigeminal and geniculate neurons. The data on passive membrane, action potential, and ion channel characteristics demonstrate clear differences between trigeminal and geniculate ganglion neurons at an embryonic stage when target tissues are innervated but receptor organs have not developed or are still immature. Therefore these electrophysiological distinctions between embryonic ganglia are present before neural activity from differentiated receptive fields can influence functional phenotype.


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