Restoration of action potential by anodal polarization in lobster giant axons

Narashashi, T

doi:10.1002/jcp.1030640108

Cited by 96 publications

(49 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…"Slow" inactivation of Na ϩ channels has been described previously in several neuronal preparations (Narahashi, 1964;Adelman and Palti, 1969;Chandler and Meves, 1970;Schauf et al, 1976;Rudy, 1978Rudy, , 1981Belluzi and Sacchi, 1986;Ogata et al, 1990;Ruben et al, 1992;Colbert and Johnston, 1996b;Fleidervish et al, 1996). In some cases the rates of both inactivation and recovery are comparably slow, whereas in other cases, as we describe here, entry into the slow inactivated state is faster than recovery from this state.…”

Section: Discussionsupporting

confidence: 74%

Prolonged Sodium Channel Inactivation Contributes to Dendritic Action Potential Attenuation in Hippocampal Pyramidal Neurons

1997

View full text Add to dashboard Cite

During low-frequency firing, action potentials actively invade the dendrites of CA1 pyramidal neurons. At higher firing rates, however, activity-dependent processes result in the attenuation of back-propagating action potentials, and propagation failures occur at some dendritic branch points. We tested two major hypotheses related to this activity-dependent attenuation of back-propagating action potentials: (1) that it is mediated by a prolonged form of sodium channel inactivation and (2) that it is mediated by a persistent dendritic shunt activated by backpropagating action potentials. We found no evidence for a persistent shunt, but we did find that cumulative, prolonged inactivation of sodium channels develops during repetitive action potential firing. This inactivation is significant after a single action potential and continues to develop during several action potentials thereafter, until a steady-state sodium current is established. Recovery from this form of inactivation is much slower than its induction, but recovery can be accelerated by hyperpolarization. The similarity of these properties to the time and voltage dependence of attenuation and recovery of dendritic action potentials suggests that dendritic sodium channel inactivation contributes to the activity dependence of action potential back-propagation in CA1 neurons. Hence, the biophysical properties of dendritic sodium channels will be important determinants of action potential-mediated effects on synaptic integration and plasticity in hippocampal neurons. Key words: dendrite; action potential; sodium channels; synaptic integration; pyramidal neuron; activity dependentRecent experiments using simultaneous somatic and dendritic patch-pipette recordings have shown that action potentials are normally initiated in the axon and back-propagate into the dendrites of many types of C NS neurons (for review, see Stuart et al., 1997). These back-propagating action potentials are likely to provide an important spatial signal that influences ongoing synaptic integration and allows for postsynaptic firing in the axon to be associated with presynaptic activity. For example, the induction of activity-dependent changes in synaptic strength such as long-term potentiation (LTP) and long-term depression depend critically on the timing of pre-and postsynaptic inputs (Levy and Steward, 1983;Markram et al., 1997), and one form of LTP has been shown to be blocked by preventing action potentials from back-propagating into the dendrites of hippocampal pyramidal neurons (Magee and Johnston, 1997). These findings demonstrate the importance of understanding the factors that determine the extent and pattern of action potential back-propagation in pyramidal neuron dendrites.Action potential back-propagation in CA1 dendrites is complex. At low frequencies action potentials invade most of the dendritic tree in an active fashion, whereas at higher frequencies action potentials attenuate more and may fail to actively propagate into much of the dendritic tree (C allaway and Ross,...

show abstract

Section: Discussionsupporting

confidence: 74%

Prolonged Sodium Channel Inactivation Contributes to Dendritic Action Potential Attenuation in Hippocampal Pyramidal Neurons

1997

View full text Add to dashboard Cite

show abstract

“…There is also a slow inactivation of the peak or readily available Na conductance, gNam3hj, similar to that observed in lobster axons by Narahashi (1964). These effects and the recovery which occurs on repolarization are described in the first part of this paper.…”

supporting

confidence: 69%

Slow changes in membrane permeability and long‐lasting action potentials in axons perfused with fluoride solutions

Chandler¹,

Meves²

1970

The Journal of Physiology

110

View full text Add to dashboard Cite

SUMMARY1. Voltage clamp experiments were carried out on squid giant axons which were perfused internally with 300 mM-NaF +sucrose and placed in K-free artificial sea-water at 16-17' C. On stepwise depolarization ( V = -38-5 to 68 mV) the Na conductance gNa rapidly reached a peak value and then declined to a new level; this 'maintained' level was slowly inactivated in an exponential manner with a rate constant which varied from 0*3 to 1.1 sec-1. This process was not influenced appreciably by replacing 50 mM-NaF with KF.2. On repolarization to a potential which varied between -73 and -101 mV the slow inactivation was removed with a rate constant of 0-11-0-73 sec-1.3. Prolonged depolarization also produced a slow inactivation of the ability of the membrane to give a transient increase in gNa. This effect developed at a rate about 1 2 that associated with the inactivation of the 'maintained' component; on repolarization, recovery of the peak 9Na was 1-2 times as fast as recovery of the 'maintained' gNa* 4. In experiments on fibres perfused with 300 mM-KF after internal NaF had removed the usual delayed K conductance, depolarization resulted in an outward current which developed in an exponential manner with a time constant of a fraction of a second. The equilibrium potential for this component was more negative than -50 mV.5. Long-lasting action potentials were computed on the basis of the above slow changes and, except for the period of final repolarization, were

show abstract

“…Internal solutions containing 150 mM-K + 150 mM-test ion decreased the peak inward currents below those predicted from independence in the amounts Na, 0-77 (see Fig. 12); Rb,Cs, Although these results might be due to a direct inhibitory action of these ions, it is also possible that they are due to a slow component of inactiva-813 814 W. K. CHANDLER AND H. MEVES tion which accompanies the decrease in resting potential and is not removed by short hyperpolarizing prepulses (Narahashi, 1964). Measurements made with 300 mM-KCl, test solution, 300 mM-KCI.…”

Section: -Exp [F(v--v'')/rt]mentioning

confidence: 84%

“…Other experiments in which small amounts of KCI were present were successful (Table 5, for example, axon 8). A possible explanation for the failure to get appreciable currents with 300 mM-NaCl is that with this solution either the low resting potential or the lack of internal potassium delays the removal of sodium inactivation under the anode (see Narahashi, 1964). Experiments designed to test this point with long anodal pulses were unsuccessful and the axons were irreversibly damaged, probably by the long hyperpolarizing currents sent through the internal electrode.…”

Section: -Exp [F(v--v'')/rt]mentioning

confidence: 99%

Voltage clamp experiments on internally perfused giant axons.

Chandler¹,

Meves²

1965

The Journal of Physiology

379

190

View full text Add to dashboard Cite

METHODS MaterialThe experiments were done during the period November 1963 to January 1964. Giant axons of 585-870 it diameter were isolated from large specimens of Loligo forbei. Living squid were available occasionally but as a rule mantles which had been stored for a few hours in ice-cold sea water were used. Extrusion and perfusionThe uncleaned axons were extruded and perfused in the way described by Baker et al (1962a). The cell in which the axons were mounted and the method of changing internal solutions were also as described in that paper. The essential features of the cell, the electrodes and the electrical equipment are illustrated in Fig. 1. Description of internal electrodeThe internal electrode consisted of a 100 , glass capillary for measuring the internal potential and a 70g platinum wire, for sending current, attached to the capillary. The 100 t glass capillary was filled with 0-6 M-KCI in contact with a silver-silver chloride electrode. A 20 , bright platinum wire ran through the capillary to reduce the high frequency impedance. The shank was filled with an agar gel of 0-6 m-KCI to prevent bulk flow of KC1 out of the electrode. The external platinum wire was insulated except for the distal 10 mm which was left bare. This part, which extended for 5 mm on either side of the tip of the glass capillary, was carefully cleaned and platinized according to the method of Moore & Cole (1963). This reduced the impedance of the wire so that an increase in voltage corresponding to a change of about 40 Q) occurred from the beginning to the end of a 10 msec

show abstract

Restoration of action potential by anodal polarization in lobster giant axons

Cited by 96 publications

References 62 publications

Prolonged Sodium Channel Inactivation Contributes to Dendritic Action Potential Attenuation in Hippocampal Pyramidal Neurons

Prolonged Sodium Channel Inactivation Contributes to Dendritic Action Potential Attenuation in Hippocampal Pyramidal Neurons

Slow changes in membrane permeability and long‐lasting action potentials in axons perfused with fluoride solutions

Voltage clamp experiments on internally perfused giant axons.

Contact Info

Product

Resources

About