Titlebook: Calcium, Neuronal Function and Transmitter Release; Proceedings of the S Rami Rahamimoff,Bernard Katz Conference proceedings 1986 Martinus

DIKE

Resting Calcium Levels and Evoked Release at the Neuromuscular Junctionnated subsequent work on this problem. We have modified their model by adding one additional parameter: the level of Ca in the resting nerve terminal. This single addition substantially alters the behavior of the model and makes it necessary to reinterpret many previous measurements. We have present

與野獸博斗者

水汽

Calcium Independent Quantal Transmitter Release at the Neuromuscular Junctionarization-transmitter secretion coupling to occur (29). Nerve impulse-evoked multi-quantal release of acetylcholine (ACh), giving rise to the end-plate potential (e.p.p.), as well as the spontaneous quantal secretion of ACh, causing the miniature end-plate potentials (m.e.p.ps), depend on extra- and

Pseudoephedrine

On the Voltage Dependence of Neurotransmitter Releaseellular Ca. concentration (3,4) resulting from terminal depolarization and inflow of calcium. Indeed, this is considered the only role of membrane depolarization; no additional effects are presumed in any of the processes that follow the entry of calcium ions and lead to the fusion of synaptic vesic

fatuity

A Possible Involvement of the Na-Ca Exchanger in Regulation of Transmitter Release at the Frog Neuronson, 1957; Dodge & Rahamimoff, 1967; Katz & Miledi, 1969; Miledi, 1973), the involvement of sodium ions in regulation of the release process — although evident since 1952 (Fatt & Katz, 1952) — is still not completely understood. Sodium ions, although cannot replace calcium in the release process it

損壞

Optical Studies of Excitation and Secretion in Vertebrate Nerve Terminalsrminals in the neurohypophyses of amphibia and mammals. Ca. and Na. contributions to the action potential are demonstrated and, in the mouse, variations in light scattering are detected following membrane potential changes known to trigger the release of peptide hormones. Calcium antagonists such as

圍巾

確定無(wú)疑

A Channel View at Ca Inactivationess is greatly reduced when outward currents are minimized. Tail currents measured at return potentials where outward currents should be negligible have envelopes that follow the rise and fall of I. and the result is readily taken as evidence of inactivation of I. (9, see also 10).

抱狗不敢前

Some Consequences of Intracellular Calcium Binding on Phasic Synaptic Transmitter Release evolved from their suggestion (2) that a residuum of “active calcium” remains within the terminal following an action potential for several milliseconds and is able to enhance the amount of transmitter released by succeeding stimuli.

grudging

https://doi.org/10.1007/978-3-322-97250-7f release results from an increase in intracellular Ca. concentrations near critical sites. Correspondingly, termination of release must result from a drop in Ca. concentration near these critical sites to levels insufficient to support release (5,6,7).