The Ionic Basis of Axonal Conduction in the Central Nervous System of Viviparus Contectus (Millet) (Gastropoda: Prosobranchia)

1972 ◽  
Vol 57 (1) ◽  
pp. 41-53
Author(s):  
D. B. SATTELLE

1. The compound action potential recorded from the pleural-supraintestinal connective of Viviparus contectus consists of a large, slow component with an average conduction velocity of about 0.02 m/sec (at 23° C) and a faster component with a conduction velocity of 0.10 m/sec (at 23° C) for the fastest fibres. 2. Both fast and slow action potentials are rapidly abolished by the substitution of tris chloride and choline chloride for the sodium salts of normal Ringer. Tetrodotoxin, applied at 10-5M rapidly abolishes action potentials in all fibres. It is, therefore, concluded that a largely sodium-dependent mechanism of spike generation operates in all axons of the connective. 3. Lithium ions effectively substitute for sodium ions in maintaining the fast action potentials for extended periods, whereas tetraethylammonium ions do not. 4. When the calcium chloride of normal Ringer is replaced by sucrose, magnesium chloride or barium chloride, conduction of fast action potentials is maintained. A small increase in the sensitivity of all axons to tetrodotoxin is observed in calcium-free Ringer; a slight reduction in the spike amplitude of fast action potentials follows the application of manganous ions at 5 mM/l in normal Ringer. It is concluded that any possible contribution of calcium to the generation of the action current of the fast action potential is very small compared to that of sodium. 5. All axons of the connective function for extended periods in sodium-free (dextran) Ringer. Under these conditions, tetrodotoxin blocks conduction in all fibres at concentrations of 10-6M, suggesting that function in dextran Ringer is maintained by a sodium-dependent mechanism.

1969 ◽  
Vol 50 (3) ◽  
pp. 711-722
Author(s):  
J. E. TREHERNE ◽  
DEFOREST MELLON ◽  
ALBERT D. CARLSON

The compound action potentials recorded in cerebro-visceral connectives consisted of a large homogeneous slow component, with a conduction velocity of between 0·03 and 0·04 m.sec-1, together with a variable rapidly conducting component, showing spikes with maximum velocities in the region of 0·4-0·5 m.sec-1. 2. Comparison of the square of the conduction velocity, for the various components of the compound action potential, with distribution of axon diameters in the connective showed that the small axons (0·1-0·3µ in diameter) contributed to the slow component, the larger axons (2·0-6·0 µ in diameter) forming the initial rapidly conducting spikes. 3. The small axons showed a rapid loss of function in preparations bathed in isotonic sucrose solutions. The larger axons, however, continued to function for appreciable periods in isotonic solutions of non-electrolytes. 4. The larger axons were rapidly and reversibly blocked by dilute tetrodotoxin. Additional evidence is also presented which suggests that the action potentials associated with the axons are sodium-dependent and do not depend upon any appreciable involvement of calcium ions in carrying the action current. 5. Both the large and the small axons appear to be relatively accessible to small ions and molecules in the bathing medium. The results are discussed in relation to the possible physiological mechanisms involved in the function of the larger axons in sodium-free solutions.


1969 ◽  
Vol 51 (2) ◽  
pp. 297-318
Author(s):  
ALBERT D. CARLSON ◽  
J. E. TREHERNE

1. The large axons in the cerebro-visceral connective have been shown to function for appreciable periods in preparations bathed in sodium-free non-electrolyte solutions. 2. The results of experiments on the effects of organic monovalent cations and anions, together with observations on the effects of tetrodotoxin, procaine and manganous ions and the changes in conduction velocity in tris chloride and dextran solutions indicate that the action potentials are, nevertheless, mediated by conventional sodium-dependent mechanisms. 3. Radioisotope experiments show that there is a small fraction, of approx. 0.5 mM/kg. tissue, which does not exchange rapidly with the 22Na in the bathing medium and which can be depleted by stimulation in sodium-free solutions. 4. On the basis of these observations it is suggested that there is sequestered extra-axonal sodium fraction which can be utilized by the large axons to maintain action potentials in preparations bathed in sodium-free solutions.


2006 ◽  
Vol 96 (6) ◽  
pp. 2963-2971 ◽  
Author(s):  
Philip M. Lang ◽  
Gila Moalem-Taylor ◽  
David J. Tracey ◽  
Hugh Bostock ◽  
Peter Grafe

Activity-dependent fluctuations in axonal excitability and changes in interspike intervals modify the conduction of trains of action potentials in unmyelinated peripheral nerve fibers. During inflammation of a nerve trunk, long stretches of axons are exposed to inflammatory mediators such as 5-hydroxytryptamine [5-HT]. In the present study, we have tested the effects of m-chlorophenylbiguanide (mCPBG), an agonist at the 5-HT(3) serotonin receptor, on activity- and potential-dependent variations in membrane threshold and conduction velocity of unmyelinated C-fiber axons of isolated rat sural nerve segments. The increase in axonal excitability during application of mCPBG was much stronger at higher frequencies of action potentials and/or during axonal membrane hyperpolarization. The effects on the postspike recovery cycle also depended on the rate of stimulation. At an action potential frequency of 1 Hz or in hyperpolarized axons, mCPBG produced a loss of superexcitability. In contrast, at 0.33 Hz, a small increase in the postspike subexcitability was observed. Similar effects on excitability changes were found when latency instead of threshold was recorded, but only at higher action potential frequencies: at 1.8 Hz, mCPBG increased conduction velocity and reduced postspike supernormality. The latter effect would increase the interspike interval if pairs of action potentials were conducted along several cm in an inflamed nerve trunk. These data indicate that activation of axonal 5-HT(3) receptors not only enhances membrane excitability but also modulates action potential trains in unmyelinated, including nociceptive, nerve fibers at high impulse rates.


1964 ◽  
Vol 206 (1) ◽  
pp. 205-210 ◽  
Author(s):  
Makoto Kobayashi ◽  
Hiroshi Irisawa

Action potentials of the smooth muscle of cat ureter were studied by using ultramicroelectrodes. Among 193 penetrations, the resting potential averaged 45 mv and the amplitude of action potential 32 mv. In four instances a slight overshoot was recorded. Action potential consisted of a relatively rapid rising phase followed by a slow repolarization phase, and its duration was about 0.3 sec. Effects of sodium deficiency on action potential were studied by using three different sodium substitutes. Both the height and the rising rate of action potential decreased as the concentration of extracellular sodium was reduced, indicating that the action potential of ureter muscle can be explained on the basis of sodium theory. The duration of the action potential was prolonged when sucrose or choline chloride was used as a sodium substitute; on the other hand, it shortened when tris chloride was employed. The essential role of sodium ions in the development of the action potential in ureter muscle is discussed.


1969 ◽  
Vol 54 (5) ◽  
pp. 607-635 ◽  
Author(s):  
Antonio Paes de Carvalho ◽  
Brian Francis Hoffman ◽  
Marilene de Paula Carvalho

Transmembrane potentials recorded from the rabbit heart in vitro were displayed as voltage against time (V, t display), and dV/dt against voltage (V, V or phase-plane display). Acetylcholine was applied to the recording site by means of a hydraulic system. Results showed that (a) differences in time course of action potential upstroke can be explained in terms of the relative magnitude of fast and slow phases of depolarization; (b) acetylcholine is capable of depressing the slow phase of depolarization as well as the plateau of the action potential; and (c) action potentials from nodal (SA and AV) cells seem to lack the initial fast phase. These results were construed to support a two-component hypothesis for cardiac electrogenesis. The hypothesis states that cardiac action potentials are composed of two distinct and physiologically separable "components" which result from discrete mechanisms. An initial fast component is a sodium spike similar to that of squid nerve. The slow component, which accounts for both a slow depolarization during phase 0 and the plateau, probably is dependent on the properties of a slow inward current having a positive equilibrium potential, coupled to a decrease in the resting potassium conductance. According to the hypothesis, SA and AV nodal action potentials are due entirely or almost entirely to the slow component and can therefore be expected to exhibit unique electrophysiological and pharmacological properties.


1965 ◽  
Vol 208 (4) ◽  
pp. 715-719 ◽  
Author(s):  
Makoto Kobayashi

Effects of Na+ and Ca++ on the generation and the conduction of excitation were studied by using a pelvis ureter specimen of cat. Action potentials were recorded simultaneously from the renal pelvis and the various regions of the ureter, and they were used to indicate the arrival of excitation. In Na+-deficient solutions, both the frequency of excitation and the conduction velocity decreased gradually, and finally a conduction block occurred at the border between the renal pelvis and ureter. In Na+-free solution spontaneous excitation was not observed in most cases. When excess Ca++ was added to Na+-free solution, spontaneous excitation was restored, but the concentration of Ca++ necessary for the restoration had to be at least twice that in normal Ringer-Krebs solution. The difference between the ureter and taenia coli was considered with regard to the role that Na+ and Ca++ play in the generation of spontaneous excitation.


1958 ◽  
Vol 36 (9) ◽  
pp. 959-975 ◽  
Author(s):  
E. E. Daniel ◽  
H. Singh

In myometrium from pregnant cat, repetitive action potentials have been recorded during contraction. Using intracellular electrodes the depolarizations averaged 35 mv. Maximum rate of depolarization was 1–2 v/sec and the action potential duration varied from 250 milliseconds to much longer periods. Membrane reversal of up to 10 mv sometimes occurred. Total resistance decreased during depolarization and recovered during repolarization. Typical biphasic potentials were also recorded with extracellular electrodes. Their amplitude (peak to peak) varied from 0.3 to several millivolts and their duration (peak to peak) from 10–40 milliseconds. Reduction of external sodium concentration to as little as one-ninth normal (choline chloride or sucrose replacement) did not reduce the amplitudes of the resting or action potentials measured intracellularly or extracellularly, but decreased the action potential frequency. Membrane reversal still occurred with intracellular electrodes and the maximum rate of depolarization was unchanged. The rate of repolarization was increased so that the total duration of the action potential was 150 to 200 milliseconds. With extracellular electrodes, the peak to peak amplitudes were increased and the durations were unchanged. Further reduction of external sodium concentration to less than 15–20 meq/liter caused a contraction without further change in action potential configuration. Gradual relaxation and slowing of the repetition rate of action potentials occurred and resulted eventually in complete mechanical and electrical inactivity.Rabbit taenia coli were also studied and their electrical properties contrasted to those of cat myometrium. The conclusions were reached that: (1) the available evidence opposes the hypotheses that an inward sodium current accounts for depolarization in smooth muscle and (2) smooth muscles differed in their electrical properties and mechanisms of ion distribution not only from striate muscles but also from one another.


1994 ◽  
Vol 72 (4) ◽  
pp. 382-393 ◽  
Author(s):  
Qi-Ying Liu ◽  
Mario Vassalle

The effects of some components of ischemia on the oscillatory (Vos) and nonoscillatory (Vex) potentials and respective currents (Ios and Iex), as well as their mechanisms, were studied in guinea pig isolated ventricular myocytes by means of a single-microelectrode, discontinuous voltage clamp method. Repetitive activations induced not only Vos and Ios, but also Vex and Iex. A small decrease in resting potential caused an immediate increase in Vos followed by a gradual increase due to the longer action potential. Immediate and gradual increases in Ios also occurred during voltage clamp steps. A small depolarization increased Vos and Vex, and facilitated the induction of spontaneous discharge by fast drive. At Vh where INa is inactivated, depolarizing steps induced larger Ios and Iex, indicating the importance of the Na-independent Ca loading. High [K]odecreased the resting potential, but also Vos, Vex, Ios, Iex, and ICa. In high [K]o, depolarization still increased Vos and Vex. Norepinephrine (NE) enhanced Vos and Vex, and also Ios and Iex, during voltage clamp steps. High [K]o antagonized NE effects, and NE those of high [K]o. In conclusion, on depolarization, Vos and Ios immediately increase through a voltage-dependent mechanism; and then Vos and Ios gradually increase, apparently through an increased Ca load related to the longer action potentials and the Na–Ca exchange. The depolarization induced by Vex may contribute to increase Vos size. Vos and Vex are similarly influenced by different procedures that modify Ca load. The arrhythmogenic events are enhanced by the simultaneous presence of depolarization, faster rate, or NE. Instead, high [K]o decreases Vos and Vex by decreasing ICa and opposes the effects of NE. The voltage clamp results show that potentiation and antagonism between different components of ischemia are due primarily to changes in Ca loading and not to changes in action potential configuration.Key words: ischemia, arrhythmias, oscillatory and nonoscillatory potentials and currents, norepinephrine, potassium.


2002 ◽  
Vol 283 (3) ◽  
pp. H1031-H1041 ◽  
Author(s):  
Gui-Rong Li ◽  
Chu-Pak Lau ◽  
Anique Ducharme ◽  
Jean-Claude Tardif ◽  
Stanley Nattel

Heart failure (HF) produces important alterations in currents underlying cardiac repolarization, but the transmural distribution of such changes is unknown. We therefore recorded action potentials and ionic currents in cells isolated from the endocardium, midmyocardium, and epicardium of the left ventricle from dogs with and without tachypacing-induced HF. HF greatly increased action potential duration (APD) but attenuated APD heterogeneity in the three regions. Early afterdepolarizations (EADs) were observed in all cell types of failing hearts but not in controls. Inward rectifier K+ current ( I K1) was homogeneously reduced by ∼41% (at −60 mV) in the three cell types. Transient outward K+ current ( I to1) was decreased by 43–45% at +30 mV, and the slow component of the delayed rectifier K+ current ( I Ks) was significantly downregulated by 57%, 49%, and 58%, respectively, in epicardial, midmyocardial, and endocardial cells, whereas the rapid component of the delayed rectifier K+ current was not altered. The results indicate that HF remodels electrophysiology in all layers of the left ventricle, and the downregulation of I K1, I to1, and I Ks increases APD and favors occurrence of EADs.


1958 ◽  
Vol 36 (1) ◽  
pp. 959-975 ◽  
Author(s):  
E. E. Daniel ◽  
H. Singh

In myometrium from pregnant cat, repetitive action potentials have been recorded during contraction. Using intracellular electrodes the depolarizations averaged 35 mv. Maximum rate of depolarization was 1–2 v/sec and the action potential duration varied from 250 milliseconds to much longer periods. Membrane reversal of up to 10 mv sometimes occurred. Total resistance decreased during depolarization and recovered during repolarization. Typical biphasic potentials were also recorded with extracellular electrodes. Their amplitude (peak to peak) varied from 0.3 to several millivolts and their duration (peak to peak) from 10–40 milliseconds. Reduction of external sodium concentration to as little as one-ninth normal (choline chloride or sucrose replacement) did not reduce the amplitudes of the resting or action potentials measured intracellularly or extracellularly, but decreased the action potential frequency. Membrane reversal still occurred with intracellular electrodes and the maximum rate of depolarization was unchanged. The rate of repolarization was increased so that the total duration of the action potential was 150 to 200 milliseconds. With extracellular electrodes, the peak to peak amplitudes were increased and the durations were unchanged. Further reduction of external sodium concentration to less than 15–20 meq/liter caused a contraction without further change in action potential configuration. Gradual relaxation and slowing of the repetition rate of action potentials occurred and resulted eventually in complete mechanical and electrical inactivity.Rabbit taenia coli were also studied and their electrical properties contrasted to those of cat myometrium. The conclusions were reached that: (1) the available evidence opposes the hypotheses that an inward sodium current accounts for depolarization in smooth muscle and (2) smooth muscles differed in their electrical properties and mechanisms of ion distribution not only from striate muscles but also from one another.


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