Prolongation of Response of Node of Ranvier by Metal Ions

Spyropoulos, C. S.; Ro, Brady

doi:10.1126/science.129.3359.1366

Cited by 20 publications

(7 citation statements)

References 17 publications

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“…The reported modulatory effects on gating of hKv1.4 may well be of physiological significance, in view of the localization of this channel in mossy fibre terminals in the hippocampus, where Zn 2+ is found in abundance (Harrison et al 1993a, b ;Huang et al 1993). In addition, low concentrations of the transition metal ion Ni 2+ dramatically prolong the action potential (Spyropoulus & Brady, 1959), and increase the response of rod channels to both cAMP and cGMP (Karpen et al 1993 ;Gordon & Zagotta, 1995).…”

Section: The Main Regulatorsmentioning

confidence: 99%

Metal ion effects on ion channel gating

Elinder

Århem

2003

Quart. Rev. Biophys.

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Metal ions affect ion channels either by blocking the current or by modifying the gating. In the present review we analyse the effects on the gating of voltage-gated channels. We show that the effects can be understood in terms of three main mechanisms. Mechanism A assumes screening of fixed surface charges. Mechanism B assumes binding to fixed charges and an associated electrostatic modification of the voltage sensor. Mechanism C assumes binding and an associated non electrostatic modification of the gating. To quantify the non-electrostatic effect we introduced a slowing factor, A. A fourth mechanism (D) is binding to the pore with a consequent pore block, and could be a special case of Mechanisms B or C. A further classification considers whether the metal ion affects a single site or multiple sites. Analysing the properties of these mechanisms and the vast number of studies of metal ion effects on different voltage-gated on channels we conclude that group 2 ions mainly affect channels by classical screening (a version of Mechanism A). The transition metals and the Zn group ions mainly bind to the channel and electrostatically modify the gating (Mechanism B), causing larger shifts of the steady-state parameters than the group 2 ions, but also different shifts of activation and deactivation curves. The lanthanides mainly bind to the channel and both electrostatically and non-electrostatically modify the gating (Mechanisms B and C). With the exception of the ether-à-go-go-like channels, most channel types show remarkably similar ion-specific sensitivities.

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Section: The Main Regulatorsmentioning

confidence: 99%

Metal ion effects on ion channel gating

Elinder

Århem

2003

Quart. Rev. Biophys.

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“…frequency, then the effects of Mg on this frequency might arise secondarily from an effect of Mg on the quantity of Na that entered the nerve terminal during a tetanus. For instance, Mg may have effects similar to Na and other divalent cations and prolong the action potential in the nerve terminal during a tetanus, thereby increasing the quantity of Na that enters with each impulse (Spyropoulos, 1956;Spyropoulos & Brady, 1959;Connelly, 1962). Our results may be compatible with any or all of these ideas, and we cannot decide among them in any conclusive manner.…”

Section: Discussionmentioning

confidence: 99%

Effects of calcium and magnesium on the frequency of miniature end‐plate potentials during prolonged tetanization

Hurlbut¹,

Longenecker²,

Mauro³

1971

The Journal of Physiology

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1. End‐plate potentials (e.p.p.s) and miniature end‐plate potentials (min.e.p.p.s) were recorded intracellularly from the cutaneous pectoris nerve‐muscle preparation of the frog during prolonged stimulation at low frequencies (5/sec—50/sec). 2. When Ca was present in the bathing solution, the quantum content of the e.p.p. and the frequency of occurrence of the min.e.p.p.s gradually increased during the period of stimulation. During the first few minutes of stimulation, the min.e.p.p. frequency increased linearly with time, and the rate of increase was dependent on the Ca concentration of the bathing solution. However, Mg had no effect on this Ca‐dependent increase in min.e.p.p. frequency. 3. A large maintained increase in min.e.p.p. frequency also occurred during prolonged stimulation in solutions that contained no added Ca and 1‐2 m M‐EGTA. Under these conditions the increase in min.e.p.p. frequency was dependent on the Mg concentration of the bathing solution and was exponential in time. 4. It is suggested that the rise in min.e.p.p. frequency is caused by an accumulation of Ca or Mg ions in the nerve terminal, and it is suggested that these ions enter the terminal at relatively non‐specific sites distinct from the Ca‐specific sites that trigger the ‘phasic’ release of transmitter.

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“…The four ions selected have been U022+ (Mambrini & Benoit, 1968), Ni2+ (Spyropoulos & Brady, 1959), Zn2+, tetraethylammonium (TEA) (Schmidt & Stimpffi, 1966) and will be referred to as 'increasing nerve spike duration ions'. These ions have the common property of producing a characteristic plateau of depolarization during the falling phase of the spike at Ranvier's node.…”

Section: Introductionmentioning

confidence: 99%

Modification of transmitter release by ions which prolong the presynaptic action potential

Benoit¹,

Mambrini²

1970

The Journal of Physiology

130

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1. The action of ions which increase the nerve spike duration at Ranvier's node has been studied at the neuromuscular junction of the frog. The duration of the presynaptic action potential is increased by UO2, Ni, Nz and TEA ions. 2. The release of transmitter after a nerve impulse is delayed and prolonged in the presence of the four ions, but the amount of evoked transmitter release estimated from the mean quantal content of e.p.p. is increased only by UO22+ and TEA. Both Ni2+ and Zn2+ decrease it. 3. The frequency of m.e.p.p.s is increased by UO22+ and decreased by Ni2+ and Zn2+ at KCl‐depolarized junctions. It is not affected by TEA. 4. It has been concluded that the increased presynaptic spike duration is responsible for the delayed and prolonged transmitter release in the presence of ions which increase the nerve spike duration at Ranvier's node. It is demonstrated that some ‘specific’ effects possibly resulting from ionic competition for presynaptic sites between UO22+, Ni2+ or Zn2+ and other ions present in the Ringer may increase, interfere with, or hide the increased transmitter release that may be predicted from the lengthened presynaptic depolarization.

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Prolongation of Response of Node of Ranvier by Metal Ions

Cited by 20 publications

References 17 publications

Metal ion effects on ion channel gating

Metal ion effects on ion channel gating

Effects of calcium and magnesium on the frequency of miniature end‐plate potentials during prolonged tetanization

Modification of transmitter release by ions which prolong the presynaptic action potential

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