Calcium Entry Leads to Inactivation of Calcium Channel in
            <i>Paramecium</i>

Brehm, Paul; Eckert, Roger

doi:10.1126/science.103199

Cited by 512 publications

(370 citation statements)

References 19 publications

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“…entry, such as Ca ?? channel inactivation (Brehm and Eckert 1978), autoreceptor activation (Nistri and Cherubini 1991;Wu and Saggau 1994) or action potential conduction failures (Krnjevic and Miledi 1958), are unlikely to significantly contribute to the depression in this study.…”

Section: Discussionmentioning

confidence: 96%

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Bui

Glavinović

2012

Cogn Neurodyn

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Short-term synaptic depression mainly reflects the depletion of the readily releasable pool (RRP) of quanta. Its dynamics, and especially the replenishment rate of the RRP, are still not well characterized in spite of decades of investigation. Main reason is that the vesicular storage and release system is treated as time-independent. If it is time-dependent all parameters thus estimated become problematic. Indeed the reports about how prolonged stimulation affects the dynamics are contradictory. To study this, we used patterned stimulation on the Schaeffer collateral fiber pathway and model-fitting of the excitatory post-synaptic currents (EPSC) recorded from CA1 neurons in rat hippocampal slices. The parameters of a vesicular storage and release model with two pools were estimated by minimizing the squared difference between the ESPC amplitudes and simulated model output. This yields the 'basic' parameters (release coupling, replenishment coupling and RRP size) that underlie the 'derived' and commonly used parameters (fractional release and replenishment rate). The fractional release increases when [Ca ?? ] o is raised, whereas the replenishment rate is [Ca ?? ] o independent. Fractional release rises because release coupling increases, and the RRP becomes less able to contain quanta. During prolonged stimulation, the fractional release remains generally unaltered, whereas the replenishment rate decreases down to *10 % of its initial value with a decay time of *15 s, and this decrease in the replenishment rate significantly contributes to synaptic depression. In conclusion, the fractional release is [Ca ?? ] odependent and stimulation-independent, whereas the replenishment rate is [Ca ?? ] o -independent and stimulation-dependent.

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Section: Discussionmentioning

confidence: 96%

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Bui

Glavinović

2012

Cogn Neurodyn

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“…cells, the largest peak phase II tail current occurred at pulse potentials between +20 and + 40 mV, and the amplitude of the current elicited by a pulse to + 100 mV ranged from 10 to 20 % of the largest current. Various neurophysiological processes which require Ca2+ influx also display an inverted U-shaped relationship with pulse potential; for example, the activation of IK(Ca) (Meech & Standen, 1975;Gorman & Thomas, 1980a), Ca2+-dependent inactivation of Ca2+ current (Brehm & Eckert, 1978;Eckert & Tillotson, 1981); and neurotransmitter release at squid central synapses (Katz & Miledi, 1967). Therefore, it seems likely that the inward current which predominates during phase II is Ca2+-activated.…”

Section: Slow Tail Currents In Bursting Neuronesmentioning

confidence: 99%

Calcium‐dependent inward current in Aplysia bursting pace‐maker neurones.

Krämer¹,

Zucker²

1985

The Journal of Physiology

124

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SUMMARY1. Depolarizing voltage-clamp pulses elicit a triphasic series of tail currents (phase I, II and III) in Aplysia burst-firing neurones L2-L6. The sequence and time course of the tail currents resemble slow changes in membrane potential which follow bursts in the unclamped cell.2. The phase II tail current is an inward current with a time course similar to that of the depolarizing after-potential (d.a.p.) which follows bursts in the unclamped cell.The phase II tail current is suppressed by depolarizing pulses which approach Eca, is blocked by Ca2+ current antagonists (Co2+ and Mn2+), and is blocked by intracellular injection of EGTA.3. The phase II tail current is not blocked by agents which block Na+-dependent action potentials, the Na+{-Ca2+ exchange pump, or the Na+-K+ exchange pump. The phase II tail current is not blocked by the elimination of large outward K+ currents which can lead to extracellular K+ accumulation. Thus, the phase II tail current is not generated by any of these processes.4. The phase II tail current is reduced by about 60 % following substitution of tetramethylammonium (TMA+) for external Na+, but is unaffected by reducing external Cl-.5. The phase II tail current is distinct from a persistent inward Ca2+ current which underlies the negative resistance region of the steady-state current-voltage relation of bursting cells. The persistent inward current is only slightly reduced by TMA+ substitution for Na+, and is enhanced by EGTA injection.6. Injection of Ca2+ into Aplysia bursting cells elicits a biphasic (inward-outward)current. The inward current can be observed in isolation after blocking the outward component (Ca2+-activated K+ current) with 50 mM-external tetraethylammonium. 7. The Ca2+-elicited inward current has a reversal potential near -22 mV, and is non-selective for Na+, K+ and Ca2+. The reversal potential is unaffected by changes in Cl-and pH. The Ca2+-activated conductance is apparently voltage independent.8. We propose that the phase II tail current, and hence the d.a.p., is due to the Ca2+-dependent activation of a voltage-independent non-specific cationic conductance. This conductance participates in generating the depolarizing phase of bursting pace-maker activity.

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“…Chad, Eckert and colleagues (Brehm and Eckert, 1978;Tillotson, 1979;Chad et al, 1984;Eckert and Chad, 1984) have demonstrated that the biphasic inactivation of this current is due to a CaZ+-dependent process. They have further shown that the ratio of the rapid to slow phase of inactivation is reduced when the current is partially block with Cd 2+ .…”

Section: Properties Of N Current Inactivationmentioning

confidence: 99%

“…The experiment of Fig. 3 employs a variation on the classic two-pulse protocol used by previous investigators to test for the presence of current-dependent inactivation (Brehm and Eckert, 1978;Eckert and Chad, 1984;Kalman, O'Lague, Erxleben, and Armstrong, 1988;Kasai and Aosaki, 1988). In this experiment, a conditioning prepulse of varying amplitude and fixed duration is followed by a short test pulse to a potential that evokes maximal current.…”

Section: Inactivation As a Function Of Prepulse Potentialmentioning

confidence: 99%

“…(b) Ca 2+-dependent inactivation (as originally described by Brehm and Eckert [1978] and Tillotson [1979]) involves transitions of channel molecules into a refractory state that is produced by binding of Ca z+ ions following their influx through open channels. HVA Ca 2+ current of molluscan neurons exhibits biphasic inactivation kinetics qualitatively similar to that of N current in chick DR(;.…”

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confidence: 99%

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Inactivation of N-type calcium current in chick sensory neurons: calcium and voltage dependence.

Cox

Dunlap

1994

The Journal of General Physiology

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We have studied the inactivation of high-voltage-activated (HVA), t0-conotoxin-sensitive, N-type Ca 2+ current in embryonic chick dorsal root ganglion (DRG) neurons. Voltage steps from -80 to 0 mV produced inward Ca ~+ currents that inactivated in a biphasic manner and were fit well with the sum of two exponentials (with time constants of ~ 100 ms and > 1 s). As reported previously, upon depolarization of the holding potential to -40 mV, N current amplitude was significantly reduced and the rapid phase of inactivation all but eliminated (Nowycky, M. C., A. P. Fox, and R. W. be explained by a model in which N channels inactivate by both fast and slow voltage-dependent processes. Alternatively, kinetic models of Ca-dependent inactivation suggest that the biphasic kinetics and holding-potential-dependence of N current inactivation could be due to a combination of Ca-dependent and slow voltage-dependent inactivation mechanisms. To distinguish between these possibilities we have performed several experiments to test for the presence of Cadependent inactivation. Three lines of evidence suggest that N channels inactivate in a Ca-dependent manner. (a) The total extent of inactivation increased 50%, and the ratio of rapid to slow inactivation increased ~ twofold when the concentration of the Ca 2 § buffer, EGTA, in the patch pipette was reduced from 10 to 0.1 mM. (b) With low intracellular EGTA concentrations (0.1 mM), the ratio of rapid to slow inactivation was additionally increased when the extracellular Ca 2 § concentration was raised from 0.5 to 5 mM. (c) Substituting Na § for Ca 2 § as the permeant ion eliminated the rapid phase of inactivation. Other results do not support the notion of current-dependent inactivation, however. Although high intraceUular EGTA (10

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Calcium Entry Leads to Inactivation of Calcium Channel in Paramecium

Cited by 512 publications

References 19 publications

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Calcium‐dependent inward current in Aplysia bursting pace‐maker neurones.

Inactivation of N-type calcium current in chick sensory neurons: calcium and voltage dependence.

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