Increased spontaneous transmitter release from presynaptic nerve terminal by methylmercuric chloride

Nature ◽  
1975 ◽  
Vol 256 (5514) ◽  
pp. 211-213 ◽  
Author(s):  
M. S. JUANG ◽  
K. YONEMURA
Keyword(s):  
Nerve Terminal ◽  
Transmitter Release ◽  
Presynaptic Nerve Terminal ◽  
Methylmercuric Chloride

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 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.

Ion Channels in Presynaptic Nerve Terminals and Control of Transmitter Release

1999 ◽  
Vol 79 (3) ◽  
pp. 1019-1088 ◽  
Author(s):  
Alon Meir ◽  
Simona Ginsburg ◽  
Alexander Butkevich ◽  
Sylvia G. Kachalsky ◽  
Igor Kaiserman ◽  
...  
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Nerve Terminal ◽  
Transmitter Release ◽  
Surface Membrane ◽  
Basic Function ◽  
Fine Tuning ◽  
Nerve Terminals ◽  
Presynaptic Nerve Terminal ◽  
Presynaptic Nerve Terminals

The primary function of the presynaptic nerve terminal is to release transmitter quanta and thus activate the postsynaptic target cell. In almost every step leading to the release of transmitter quanta, there is a substantial involvement of ion channels. In this review, the multitude of ion channels in the presynaptic terminal are surveyed. There are at least 12 different major categories of ion channels representing several tens of different ion channel types; the number of different ion channel molecules at presynaptic nerve terminals is many hundreds. We describe the different ion channel molecules at the surface membrane and inside the nerve terminal in the context of their possible role in the process of transmitter release. Frequently, a number of different ion channel molecules, with the same basic function, are present at the same nerve terminal. This is especially evident in the cases of calcium channels and potassium channels. This abundance of ion channels allows for a physiological and pharmacological fine tuning of the process of transmitter release and thus of synaptic transmission.

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.

Pertussis toxin effects on transmitter release from perivascular nerve terminals

1989 ◽  
Vol 256 (2) ◽  
pp. H455-H459 ◽  
Author(s):  
M. Nozaki ◽  
N. Sperelakis
Keyword(s):  
Pertussis Toxin ◽  
Nerve Terminal ◽  
Transmitter Release ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Nerve Terminals ◽  
Temperature Dependent ◽  
Presynaptic Nerve Terminal ◽  
Excitatory Junction Potentials ◽  
Sympathetic Nerve Terminal

Pertussis toxin (PT) was used to investigate the possible involvement of an inhibitory GTP-binding protein (G protein) in neuromuscular transmission at the sympathetic nerve terminal of guinea pig mesenteric artery. When the intracellular microelectrode technique was used, the amount of transmitter released was evaluated by recording the amplitude of excitatory junction potentials (EJPs) in the vascular smooth muscle (VSM) cells. EJPs were evoked by perivascular nerve stimulation with brief square pulses. The amplitude of EJPs was depressed by exogenously applied norepinephrine (NE) (greater than or equal to 10(-7) M) or histamine (greater than or equal to 10(-7) M). However, these effects of NE and histamine on EJP amplitude were almost completely blocked in PT-pretreated VSM cells (2 x 10(-7) g/ml PT, 24 h at 21 degrees C). These effects of PT pretreatment were time and temperature dependent. In contrast, there was no significant change in the resting membrane potential (-70.1 +/- 2.1 mV) or input resistance (11.9 +/- 0.4 M omega) in the VSM cells after PT pretreatment. These results suggest that the effects of NE and histamine on EJP amplitude may be mediated by PT-sensitive G proteins in the presynaptic nerve terminal.

Local synthesis of nuclear-encoded mitochondrial proteins in the presynaptic nerve terminal

2001 ◽  
Vol 64 (5) ◽  
pp. 447-453 ◽  
Author(s):  
Anthony E. Gioio ◽  
Maria Eyman ◽  
Hengshan Zhang ◽  
Zeno Scotto Lavina ◽  
Antonio Giuditta ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Mitochondrial Proteins ◽  
Local Synthesis ◽  
Presynaptic Nerve Terminal

scholarly journals Cumulative and persistent effects of nerve terminal depolarization on transmitter release

1973 ◽  
Vol 228 (2) ◽  
pp. 407-434 ◽  
Author(s):  
J. D. Cooke ◽  
D. M. J. Quastel
Keyword(s):  
Nerve Terminal ◽  
Transmitter Release

scholarly journals Synuclein: a neuron-specific protein localized to the nucleus and presynaptic nerve terminal

1988 ◽  
Vol 8 (8) ◽  
pp. 2804-2815 ◽  
Author(s):  
L Maroteaux ◽  
JT Campanelli ◽  
RH Scheller
Keyword(s):  
Nerve Terminal ◽  
Specific Protein ◽  
Presynaptic Nerve Terminal
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