The calyx-type synapse of the chick ciliary ganglion as a model of fast cholinergic transmission

1992 ◽  
Vol 70 (S1) ◽  
pp. S73-S77 ◽  
Author(s):  
E. F. Stanley
Keyword(s):  
Calcium Channels ◽  
Nerve Terminal ◽  
Transmitter Release ◽  
Action Potentials ◽  
Calcium Currents ◽  
Ciliary Ganglion ◽  
Presynaptic Nerve Terminal ◽  
And Control ◽  
Single Calcium Channels ◽  
Experimental Preparation

The calyx-type synapse of the embryonic chick ciliary ganglion is reviewed as a model of transmitter release from a vertebrate presynaptic nerve terminal. This nerve terminal is extensive in area, enabling the penetration with microelectrodes and the application of patch-clamp techniques. In other respects the calyx synapse is a typical fast-transmitting cholinergic nerve terminal. This synapse has been used to obtain the first recordings of action potentials and calcium currents in a vertebrate presynaptic nerve terminal and is the only preparation in which it has proved possible to record single calcium channels directly from the transmitter release sites. The calyx remains a powerful experimental preparation for the further analysis of the mechanism and control of neurotransmitter release in fast-transmitting nerve terminals.Key words: synaptic transmission, presynaptic, transmitter release, acetylcholine release, calcium channels.

scholarly journals The Frog Motor Nerve Terminal Has Very Brief Action Potentials and Three Electrical Regions Predicted to Differentially Control Transmitter Release

2020 ◽  
Vol 40 (18) ◽  
pp. 3504-3516 ◽  
Author(s):  
Scott P. Ginebaugh ◽  
Eric D. Cyphers ◽  
Viswanath Lanka ◽  
Gloria Ortiz ◽  
Evan W. Miller ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Transmitter Release ◽  
Action Potentials ◽  
Motor Nerve ◽  
Motor Nerve Terminal

Primary and Secondary Regulation of Quantal Transmitter Release: Calcium and Sodium

1980 ◽  
Vol 89 (1) ◽  
pp. 5-18
Author(s):  
RAMI RAHAMIMOFF ◽  
AHARON LEV-TOV ◽  
HALINA MEIRI
Keyword(s):  
Action Potential ◽  
Nerve Terminal ◽  
Transmitter Release ◽  
Surface Membrane ◽  
Nerve Impulse ◽  
High Frequency Stimulation ◽  
Extracellular Medium ◽  
Presynaptic Nerve Terminal ◽  
Virtual Absence ◽  
Frequency Stimulation

Calcium is the prime regulator of quantal acetylcholine liberation at the neuromuscular junction; its entry through the presynaptic membrane and the level of free [Ca]ln most probably determine the number of transmitter quanta liberated by the nerve impulse. The level of free [Ca]ln, in turn, is controlled by a number of subcellular elements: mitochondria, endoplasmic reticulum, vesicles, macromolecules and the surface membrane. The action potential induced calcium entry is not the only factor responsible for coupling nerve terminal depolarization with increased transmitter release; increased transmitter release occurs also in the virtual absence of calcium ions in the extracellular medium, when a reversed electrochemical gradient for calcium probably exists during action potential activity. Several lines of evidence suggest that the entry of sodium ions is responsible for this augmented transmitter release: the tetanic potentiation observed under reversed calcium gradient is blocked by tetrodotoxin; tetanic and post-tetanic potentiation are augmented and prolonged by ouabain; the amplitude of the extracellular nerve action potential is reduced with high-frequency stimulation, in parallel with increased spontaneous quantal release. In addition, sodium-filled egg-lecithine liposomes augment quantal liberation. The augmentory effect of sodium on transmitter release is probably due to an intracellular calcium translocation, since no preferred timing after the action potential is observed. Thus the level of [Na]ln in the presynaptic nerve terminal can control indirectly the efficiency of synaptic transmission.

Transmitter release induced by injection of calcium ions into nerve terminals

1973 ◽  
Vol 183 (1073) ◽  
pp. 421-425 ◽  
Keyword(s):  
Nerve Terminal ◽  
Calcium Ions ◽  
Transmitter Release ◽  
Nerve Terminals ◽  
Presynaptic Nerve Terminal ◽  
External Fluid ◽  
Giant Synapse ◽  
Evoked Transmitter Release

Calcium ions injected into the presynaptic nerve terminal in the giant synapse of the squid, evoked transmitter release while similar doses of Mg and Mn were ineffective. The transmitter release induced by intracellular application was still observed when Ca was replaced in the external fluid by Mn, in spite of the fact that this abolished transmitter release in response to presynaptic depolarization.

scholarly journals Localization of individual calcium channels at the release face of a presynaptic nerve terminal

Neuron ◽  
1994 ◽  
Vol 13 (6) ◽  
pp. 1275-1280 ◽  
Author(s):  
Philip G. Haydon ◽  
Eric Henderson ◽  
Elis F. Stanley
Keyword(s):  
Calcium Channels ◽  
Nerve Terminal ◽  
Presynaptic Nerve Terminal

scholarly journals Multitude of ion channels in regulation of transmitter release

1999 ◽  
Vol 354 (1381) ◽  
pp. 281-288 ◽  
Author(s):  
Rami Rahamimoff ◽  
Alexander Butkevich ◽  
Dessislava Duridanova ◽  
Ronit Ahdut ◽  
Emanuel Harari ◽  
...  
Keyword(s):  
Ion Channels ◽  
Potassium Channels ◽  
Nerve Terminal ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Chloride Channels ◽  
Surface Membrane ◽  
Structural Basis ◽  
Primary Role ◽  
Presynaptic Nerve Terminal

The presynaptic nerve terminal is of key importance in the communication in the nervous system. Its primary role is to release transmitter quanta on the arrival of an appropriate stimulus. The structural basis of these transmitter quanta are the synaptic vesicles that fuse with the surface membrane of the nerve terminal, to release their content of neurotransmitter molecules and other vesicular components. We subdivide the control of quantal release into two major classes: the processes that take place before the fusion of the synaptic vesicle with the surface membrane (the pre–fusion control) and the processes that occur after the fusion of the vesicle (the post–fusion control). The pre–fusion control is the main determinant of transmitter release. It is achieved by a wide variety of cellular components, among them the ion channels. There are reports of several hundred different ion channel molecules at the surface membrane of the nerve terminal, that for convenience can be grouped into eight major categories. They are the voltage–dependent calcium channels, the potassium channels, the calcium–gated potassium channels, the sodium channels, the chloride channels, the non–selective channels, the ligand gated channels and the stretch–activated channels. There are several categories of intracellular channels in the mitochondria, endoplasmic reticulum and the synaptic vesicles. We speculate that the vesicle channels may be of an importance in the post–fusion control of transmitter release.

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