The role of calcium ions in the action potentials of Helix aspersa neurones

Kerkut, G.A.; Gardner, D.R.

doi:10.1016/0010-406x(67)90730-x

Cited by 105 publications

(22 citation statements)

References 24 publications

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“…Increase in potassium comductance following barium injection Addition of barium chloride to the bathing medium produces prolonged action potentials in Helix neurones and, if the external calcium is entirely replaced by barium, repolarization of the action potential may be delayed for 30-40 sec (Kerkut & Gardner, 1967). This could be accounted for if the barium inward current failed to activate the repolarizing potassium current which is normally induced by calcium influx (Meech, 1976) and it is.…”

Section: Discussionmentioning

confidence: 99%

Effect of measured calcium chloride injections on the membrane potential and internal pH of snail neurones.

Meech¹,

Thomas²

1980

The Journal of Physiology

136

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SUMMARY1. Ion-sensitive micro-electrodes were used to measure changes in intracellular pH (pH,) and internal chloride which resulted from the pressure injection of calcium chloride into identified Helix aspersa neurones. The-internal chloride measurement allowed the quantity of calcium chloride injected to be estimated.2. Application of the metabolic inhibitor carbonyl cyanide m-chlorophenyl hydrazone (CCmP) to a calcium-loaded cell caused an increase in the membrane potential comparable to the effect of injecting calcium itself. The effect was not observed in normal cells.3. When injected in the presence of C(mp, calcium caused a much larger and longer-lasting effect on the membrane potential than that observed in untreated cells.4. The injection of ruthenium red can increase and/or prolong the hyperpolarization caused by a given quantity of injected calcium. The pH, changes following calcium injection were biphasic and slower than normal. 5. In seven experiments, both hydrogen chloride and calcium chloride were injected into the same cell. The relative changes in pHi corresponded to the production of one hydrogen ion for each calcium ion injected. 6. The relationship between the quantity of calcium injected and the size of the induced hyperpolarization suggested that at least three calcium ions acting cooperatively are required to activate a potassium 'channel'. 7. Injection of barium chloride hyperpolarized the membrane after a delay of about 1 min. After several injections of barium the cell lost this response while retaining its normal response to calcium injection. Injection of barium also caused a slowly developing (biphasic) fall in pHi.8. We conclude that injected calcium is normally rapidly taken up by mitochondria in exchange for hydrogen ions. If this uptake process is blocked by ruthenium red or CCmP, the calcium is taken up by a second, slower, process which also releases hydrogen ions. When pre-loaded, but not otherwise, the mitochondria will release * Present address:

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Section: Discussionmentioning

confidence: 99%

Effect of measured calcium chloride injections on the membrane potential and internal pH of snail neurones.

Meech¹,

Thomas²

1980

The Journal of Physiology

136

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“…The Ca channels in many other types of cells are, however, impermeable to Mn (e.g. Hagiwara & Nakajima, 1966;Kerkut & Gardner, 1967). Thus the Ca channel, unlike the Na channel, has very dissimilar ionic selectivities in different preparations (for review see Edwards, 1982).…”

Section: Mn Andneurotransmitter Releasementioning

confidence: 99%

“…Mn, a first-series transition metal, has complicated effects on neurosecretion. Although it inhibits the nerve-evoked release of transmitter (Katz & Miledi, 1969;Meiri & Rahamimoff, 1972) and blocks many Ca channels (Hagiwara & Nakajima, 1966;Kerkut & Gardner, 1967), it can, in the absence of external Ca, increase the frequency of quantal release following tetanic nerve stimulation (Kita, Narita & Van der Kloot, 1981). In addition, Mn produces a long-lasting potentiation ofacetylcholine (ACh) release from cardiac parasympathetic nerve endings (Bechem, Glitsch & Pott, 1981).…”

Section: Introductionmentioning

confidence: 99%

Manganese fluxes and manganese‐dependent neurotransmitter release in presynaptic nerve endings isolated from rat brain.

Drapeau¹,

Nachshen²

1984

The Journal of Physiology

175

123

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SUMMARY1. The uptake and efflux of 54Mn and 45Ca, and the release of dopamine (DA) were measured in pinched-off presynaptic nerve endings (synaptosomes) isolated from rat brain.2. The uptake of Mn and Ca was increased when forebrain or striatal synaptosomes were incubated in a depolarizing, K-rich solution. The time courses of K-stimulated Mn and Ca entry were similar: there was initially a high rate of ion accumulation, lasting 1-3 s, that gradually levelled off. The initial uptake of Mn, like that of Ca, was greatly diminished by a 10 s pre-incubation in K-rich solution prior to the addition of radiotracer.3. Several Ca channel blockers, including Ni (0 03 mM), Sr (2'0 mM), Co (0 04 mM), Ba (1-5 mM) and La (0-2 mM), suppressed the K-stimulated uptake of Mn and of Ca to a similar extent. The K-stimulated uptake of Mn increased as a function of the external Mn concentration, and saturated at high external concentrations of Mn. These high concentrations of Mn also blocked the K-stimulated uptake of Ca.4. There was a decreased efflux of Ca, but not of Mn, from the synaptosomes when the external Na concentration was reduced. The Na-dependent efflux of Ca was diminished by external Mn, but was unaffected when the synaptosomes were loaded with Mn.5. The rate of [3H]DA release from striatal synaptosomes was less than 0-001 sin non-depolarizing, low-K solutions, in the absence or presence of Mn and Ca (1 mM). The rate ofrelease was also unchanged in depolarizing, K-rich solutions in the absence of these divalent cations. The addition of 1 mM-Mn to a K-rich solution increased the rate of DA release by about 40 %, and the time course of release was linear for at least 30 s. The addition of t mM-Ca increased the rate of release nearly 100-fold during the first second, and thereafter the rate of release rapidly declined.6. Ni (1 mM) and, to a lesser extent, Mg (10 mM) reduced the rate of K-stimulated DA release that is dependent on either Mn or Ca. The pattern of inhibition of DA release resembled the pattern of inhibition of K-stimulated uptake of Mn and Ca.

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“…Therefore, it was felt that analysis of the mode of action of the organic Ca2k-antagonists should be carried out in a preparation in which pure Ca2+ current can be separated from other ionic currents in the excitable membrane. In this respect, the snail neurone in which voltage-dependent currents carried by Ca2+, Na+ and K+ have been identified, seems to be the most suitable preparation for analysis of drugaction (Kerkut & Gardner, 1967;Geduldig & Gruener, 1970;Standen, 1975;Kostyuk, Krishtal & Pidoplichko, 1975; Akaike, , and furthermore, in this preparation pure Ca2+ current can be separated for other ionic currents with a suction pipette technique recently developed by our laboratory which allows internal perfusion of the cell body and voltage clamp Akaike et al, 1978). Therefore, the present experiments were designed in an attempt to examine the effects of verapamil, and diltiazem which has been introduced as an organic Ca2+-antagonist (Sato, t) Macmillan Publishers Ltd 1981 Nagao, Yamaguchi, Nakajima & Kiyomoto, 1971;Nagao, Sato, Nakajima & Kiyomoto, 1972;Nikajima, Hoshiyama, Yamashita & Kiyomoto, 1975) (Akaike, Lee & Brown, 1979).…”

Section: Introductionmentioning

confidence: 99%

ACTIONS OF VERAPAMIL, DILTIAZEM AND OTHER DIVALENT CATIONS ON THE CALCIUM‐CURRENT OF Helix NEURONES

Akaike

Brown

Nishi

et al. 1981

British J Pharmacology

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1 Effects of organic verapamil and diltiazem, and cations, Ni2+, Mn2+, Co2+ and La3`on Ca2+ current (ICa) separated from other ionic currents in a Helix neurone were studied. A suction pipette technique which allows internal perfusion of the cell body and voltage clamp was used.2 Verapamil and diltiazem (10-6 10-4M) increased the threshold, and decreased both the amplitude and rate of rise of the soma Ca2+-spike. Both agents inhibited ICa over the entire range of the current-voltage (I-V) relationship dose-dependently, without shifting the threshold of the I-V relationship. Increases in external Ca2+ overcame the inhibitory action of the agents. 3 Divalent cations, Ni2+, Mn2+, Co2+ and the trivalent cation, La3+ inhibited ICa dosedependently, but induced shifts of the I-V relationship to more positive voltages. The order of potency of inhibition of ICa among these cations was as follows; Ni2+ > La3+ > Mn2+ > Co2+. 4 Double reciprocal plots for peak ICa versus external Ca2+ concentrations in the presence or absence of both organic and inorganic Ca2+-antagonists intersect at the ordinate. Results indicate that both organic and inorganic Ca2+-antagonists compete for Ca2+ at the common binding site for Ca2+.5 Internal application of the organic Ca2+-antagonists (10-4M) inhibited ICa in a time-dependent manner to about 40-60% of the control. Ni2+, when applied internally, also depressed ICa* 6 The results provide evidence that organic Ca2+-antagonists occupy the binding site for Ca2+ in a competitive manner at the surface of the soma membrane of the Helix neurone, while divalent and trivalent cations, in addition to inhibiting ICa in a similar manner to the organic Ca2+_antagonists, change the surface charge of the soma membrane.

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The role of calcium ions in the action potentials of Helix aspersa neurones

Cited by 105 publications

References 24 publications

Effect of measured calcium chloride injections on the membrane potential and internal pH of snail neurones.

Effect of measured calcium chloride injections on the membrane potential and internal pH of snail neurones.

Manganese fluxes and manganese‐dependent neurotransmitter release in presynaptic nerve endings isolated from rat brain.

ACTIONS OF VERAPAMIL, DILTIAZEM AND OTHER DIVALENT CATIONS ON THE CALCIUM‐CURRENT OF Helix NEURONES

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