An aequorin study of a facilitating calcium current in bursting pacemaker neurons of Helix

Lux, H. D.; Heyer, C.B.

doi:10.1016/0306-4522(77)90054-9

Cited by 31 publications

(18 citation statements)

References 20 publications

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“…Several voltage clamp studies of repetitive pulses have been interpreted in this way (Heyer & Lux, 1976a;Lux & Heyer, 1977;. For dorid neurones we have found no evidence to support facilitation of Ca conductance during repetitive activity at frequencies slower than 1 Hz.…”

Section: Role Of Ca Currentmentioning

confidence: 75%

“…It is seen in Na-free-TEA saline but not in Ca-free-Co plus TEA saline. It corresponds to the maintained Ca current observed in molluscan cells by Adams & Gage (1976), Connor (1977), Eckert & Lux (1976), Kostyuk, Krishtal & Pidoplichko (1975), and shows a marked similarity to the Ca current observed in the presynaptic terminal of the squid giant synapse by Llina's, Steinberg & Walton (1976 (Meech & Standen, 1975;Thompson, 1977 (Heyer & Lux, 1976a;Lux & Heyer, 1977;Eckert, Tillotson & Ridgway, 1977). It is important, therefore, to determine whether a use-dependent change in maintained Ca current can be detected in direct measures of inward current.…”

Section: Broadening Of Somatic Spikementioning

confidence: 99%

See 1 more Smart Citation

Mechanism of frequency‐dependent broadening of molluscan neurone soma spikes.

Aldrich¹,

Getting²,

Thompson³

1979

The Journal of Physiology

159

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inward Ca currents show significant spike broadening. Spike broadening apparently results from the frequency dependent inactivation of 1K which increases the expression of inward Ca current as a prominent shoulder on the repolarizing phase of the action potential. In addition, the presence of a prolonged Ca current increases the duration of the first action potential thereby allowing sufficient time for inactivation of IK.

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Section: Role Of Ca Currentmentioning

confidence: 75%

Section: Broadening Of Somatic Spikementioning

confidence: 99%

Mechanism of frequency‐dependent broadening of molluscan neurone soma spikes.

Aldrich¹,

Getting²,

Thompson³

1979

The Journal of Physiology

159

View full text Add to dashboard Cite

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“…Other studies have suggested the presence of facilitation, but they used indirect and, therefore, relatively inconclusive methods (13)(14)(15)(16) Mechanism of Facilitation. Our results support an earlier conclusion (6) that facilitation reflects an intrinsic reaction of Ca2+ channels to changes in membrane potential because large P1 depolarizations produce facilitation even though divalent ion influx must be suppressed at very positive P1.…”

Section: Discussionmentioning

confidence: 99%

Facilitation of Ca2+-channel currents in bovine adrenal chromaffin cells.

Hoshi¹,

Rothlein²,

Smith³

1984

Proc. Natl. Acad. Sci. U.S.A.

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Ca2+-channel currents in primary cultures of bovine adrenal chromaffin cells were studied using the whole-cell patch-clamp method. Parameters of a double-pulse protocol were systematically varied to characterize facilitation by a prepulse (PI) of Ca2+-channel current during a test pulse (P2). The pulses were usually separated by 30 msec, an interval sufficient for decay of any measurable P1 tail currents. The Ca2+-channel current amplitude during P2 increased when P1voltage was more positive than 0 mV. The effect became progressively greater with more positive P1 voltage. With a 60-msec P1 to +80 mV, the current amplitude typically increased by 25%-35% during a 60-msec P2. Comparison of facilitated and control inward Ca2+-channel current I(V) curves showed that facilitation was also strongly dependent on P2 test voltage.Facilitation of Ca2+-channel currents is a voltage-dependent phenomenon and is not dependent on Ca2+ entry. When short repetitive voltage-clamp pulses were applied, the Ca2+-channel current amplitude increased with each pulse. This suggests that Ca2+-channel facilitation could enhance release of catecholamines from chromaffin cells during a train of action potentials.At many synapses, when two action potentials separated by a short interval arrive at the presynaptic terminal, the second action potential releases more transmitter than the first. This phenomenon is referred to as monosynaptic facilitation of transmitter release, and it represents one of the most common types of synaptic plasticity (1). Two major hypotheses for the mechanism of synaptic facilitation have been proposed. One states that Ca2+ channels facilitate in response to a prior depolarization. According to this hypothesis, the first action potential changes properties of the Ca2+ channels such that more Ca2+ ions flow through the channels during the second action potential, resulting in enhanced release. Ca2+ current in bovine adrenal chromaffin cells was increased by a prior depolarization pulse. This phenomenon is of special interest because this is one of the mechanisms hypothesized for synaptic facilitation. Thus, we have defined this effect of a prior depolarization pulse as facilitation of Ca2+ channels and systematically investigated the phenomenon using essentially the same chromaffin cell preparation used by Fenwick et al. We report conditions that enhance Ca2'-channel facilitation and describe its dependence on time and voltage dimensions of paired-pulse commands. The results suggest that Ca2'-channel facilitation is caused by intrinsic reactions of Ca2'-channel molecules to changes in the membrane potential and that it could be an underlying mechanism of facilitation of transmitter release in some synapses during a train of action potentials. MATERIALS AND METHODSCell Culture. Chromaffin cells were prepared from adult and young bovine adrenal medulla by the method of Kilpatrick et al. (7) as modified by Wilson and Viveros (8). The cells were plated on coverslips coated with collagen at a density of "1200 cells...

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“…There is indirect evidence that the Ca2+ current can be facilitated from measurements of the K+ current (Heyer & Lux, 1976) and from measurements of the aequorin light signal (Eckert et al 1977;Lux & Heyer, 1977) during repetitive stimulation under voltage clamp conditions. Fig.…”

Section: Inactivation and Facilitationmentioning

confidence: 99%

Intracellular calcium accumulation during depolarization in a molluscan neurone.

Gorman¹,

Thomas²

1980

The Journal of Physiology

109

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2. Dye absorbance increased linearly for depolarizing pulse durations up to 100 msec and approximately linearly between 100 and 300 msec, but for longer durations the absorbance change decreased.3. The absorbance change vs. voltage relation increased steeply between -20 and 0 mV (e-fold per 8-5 mV), peaked at + 36 mV and declined non-linearly to an estimated null or suppression potential of about + 139 mV.4. TTX (5 x 10-5 M) had no effect on the change in dye absorbance produced by brief or long duration stimuli whereas Ca2+ free ASW abolished all changes in dye absorbance.5

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An aequorin study of a facilitating calcium current in bursting pacemaker neurons of Helix

Cited by 31 publications

References 20 publications

Mechanism of frequency‐dependent broadening of molluscan neurone soma spikes.

Mechanism of frequency‐dependent broadening of molluscan neurone soma spikes.

Facilitation of Ca2+-channel currents in bovine adrenal chromaffin cells.

Intracellular calcium accumulation during depolarization in a molluscan neurone.

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