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 Synaptic structural complexity as a factor enhancing probability of calcium-mediated transmitter release

1996 ◽  
Vol 75 (6) ◽  
pp. 2451-2466 ◽  
Author(s):  
R. L. Cooper ◽  
J. L. Winslow ◽  
C. K. Govind ◽  
H. L. Atwood
Keyword(s):  
Nerve Terminal ◽  
Calcium Ion ◽  
Active Zone ◽  
Transmitter Release ◽  
Structural Complexity ◽  
Ion Concentration ◽  
Freshwater Crayfish ◽  
Channel Current ◽  
Active Zones ◽  
Calcium Ion Concentration

1. In a model synaptic system, the excitatory neuromuscular junction of the freshwater crayfish, the nerve terminals possess synapses that vary in structural complexity, with numbers of active zones ranging from zero to five. Active zones on individual synapses show a wide range of separation distances. We tested the hypothesis that two active zones of a single synapse in close proximity can enhance the localized increase in free calcium ion concentration, thus enhancing the probability of neurotransmission at that synapse. We evaluated the increase in calcium ion concentration as a function of distance between adjacent active zones. 2. To test this hypothesis, a reaction-diffusion model for Ca2+ entering the presynaptic terminals was used. This test was used because 1) present measurement techniques are inadequate to resolve quantitatively the highly localized, transient calcium microdomains at synaptic active zones; and 2) there is presently no suitable preparation for physiological recording from isolated synapses with varying distances between active zones. Included in the model were intracellular buffer and a typical distribution of voltage-activated Ca2+ channels for an active zone, estimated from freeze-fracture micrographs. 3. The model indicated that localized Ca2+ clouds from discrete active zones can overlap to create spatial enhancement of Ca2+ concentration. The degree of interaction between two active zones depends on the distance between them. When two typical active zones are separated by < or = 200 nm, the maximum intracellular Ca2+ concentration ([Ca2+]i) is greater at 1) the midpoint between them, and 2) the center of each one, than at the corresponding positions for a single isolated active zone. Enhanced [Ca2+]i at the edge of the active zone where “docked” synaptic vesicles occur would be expected to have an effect on transmitter release. 4. When the model includes no intracellular buffer, the increase in [Ca2+]i is a linear function of calcium channel current, but is a nonlinear function of the number of conducting calcium channels in an active zone. With immobile buffer included, the increase in [Ca2+]i is nonlinear with respect to both channel current and number of conducting channels. 5. Inclusion of immobile buffer in the model provides “released” residual calcium that slowly accumulates during a train of current pulses. Released residual calcium accumulates more rapidly at paired active zones separated by < or = 200 nm that at single isolated active zones. 6. We propose that the probability of release is enhanced at synapses with closely associated active zones. Synapses of this type (“complex” synapses) could be selectively recruited when the neuron is active at low frequencies. At higher frequencies of neuronal activity, more distant active zones may interact and acquire a greater probability of releasing quanta. This would provide the nerve terminal with one component of a mechanism for frequency facilitation, because the number of quanta released by the terminal as a whole would increase with frequency. Thus variation in synaptic complexity in a nerve terminal provides a mechanism for short-term plasticity of transmitter release.

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

Depolarization reverses age-related decrease of spontaneous transmitter release

1991 ◽  
Vol 70 (5) ◽  
pp. 2066-2071 ◽  
Author(s):  
W. B. Alshuaib ◽  
M. A. Fahim
Keyword(s):  
Nerve Terminal ◽  
Transmitter Release ◽  
Nerve Terminals ◽  
Tetraacetic Acid ◽  
Ca Channels ◽  
Age Related ◽  
High K ◽  
Voltage Dependent ◽  
K Concentration ◽  
Period Of Oscillation

The effect of increasing extracellular Ca concentration on spontaneous transmitter release was studied at soleus nerve terminals of young (10 mo) and old (24 mo) C57BL/6J mice depolarized by high extracellular K concentration ([K]o). By using intracellular recording, miniature end-plate potentials (MEPPs) were first recorded in a normal [K]o Krebs solution. Subsequently, MEPPs were recorded in high [K]o Krebs solutions with four different Ca concentrations: Ca-free/ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and 0.5, 1.5, and 2.5 mM Ca. In both the normal [K]o Krebs and the Ca-free-high [K]o Krebs solutions, MEPP frequency was lower at old than at young nerve terminals. In the three high [K]o Krebs solutions with Ca, MEPP frequency was progressively higher at old than at young nerve terminals with higher Ca concentrations. Periodic oscillations were observed in MEPP frequency of depolarized nerve terminals. The period of oscillation was inversely proportional to spontaneous transmitter release. These results demonstrate that when the nerve terminal is depolarized, permeability of the terminal membrane to Ca increases because of opening of voltage-dependent Ca channels. In the present study resting MEPP frequency was lower at old than at young terminals. On depolarization, MEPP frequency became higher at old than at young terminals. The study demonstrates that voltage-dependent Ca entry increases during aging at the soleus 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.

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