scholarly journals QUANTITATIVE ASPECTS OF TRANSMITTER RELEASE

1970 ◽  
Vol 47 (3) ◽  
pp. 585-592 ◽  
Author(s):  
George D. Bittner ◽  
Donald Kennedy
Keyword(s):  
Motor Neuron ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Inhibitory Neuron ◽  
Release Mechanism ◽  
Quantal Content ◽  
Vesicle Membrane ◽  
Release Process ◽  
Membrane Materials ◽  
Order Of Magnitude

The opener-stretcher motor neuron in crayfish makes 50 endings upon each of 1200 muscle fibers. We have calculated the quantal content of junctional potentials produced by individual terminals and by the whole cell at various physiological frequencies. The results show that when the motor neuron is active at 20 impulses/second, it releases 50 quanta/impulse per muscle fiber, or a total of 4.5 x 109 quanta/hr. These figures are similar to those for vertebrate muscles per fiber, but larger for the entire neuron because the opener motor unit is so large. On the basis that the quanta correspond to synaptic vesicles each containing 103–104 molecules of transmitter, the release rate must be around 10-11 mole/hr. This value is within an order of magnitude of the release figures obtained for mammalian neurons by collecting transmitter in perfusates, but it is far lower than the value reported for a crustacean inhibitory neuron. If the membrane materials surrounding each vesicle were lost in the release process, the replacement synthesis would involve 24 mm2 of membrane/hr. We conclude that the metabolic load in terms of transmitter synthesis is probably sustainable, but that the release mechanism must operate in such a way that vesicle membrane materials are neither lost nor incorporated into the terminal membrane.

scholarly journals Peroxidase uptake by photoreceptor terminals of the skate retina.

1976 ◽  
Vol 70 (1) ◽  
pp. 86-96 ◽  
Author(s):  
H Ripps ◽  
M Shakib ◽  
E D MacDonald
Keyword(s):  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Light Adaptation ◽  
Ringer Solution ◽  
Bathing Solution ◽  
Synaptic Terminal ◽  
Vesicle Membrane ◽  
Electrical Potentials ◽  
Membrane Bound ◽  
Peroxidase Uptake

The photoreceptors of dark-adapted skate retinas bathed in a Ringer solution containing horseradish peroxidase (HRP) incorporate the tracer into membrane-bound compartments within the synaptic terminal of the cell; after 1 or 2 h of incubation, approx. 10-38% of the synaptic vesicles were labeled. The receptors appeared to be functioning normally throughout the incubation period, since electrical potentials of normal amplitude could be elicited in response to dimphotic stimuli. However, it was possible to block the uptake of peroxidase by a regimen of light adaptation that effectively suppressed light-induced activity in the electroretinogram. If, during incubation with peroxidase, retinas were exposed at 10-min intervals to an intense 1-ms flash from a xenon discharge tube, the receptor terminals were almost completely devoid of peroxidase; fewer than 2% of the vesicles were labeled. The suppression of HRP uptake could also be achieved in dark-adapted retinas by adding magnesium to the bathing solution, suggesting that calcium is necessary for transmitter release from vesicles in the receptor terminals. These findings are consistent with the view that vertebrate photoreceptors discharge a neurotransmitter in darkness, and that light decreases the release of this substance. It seems likely that the incorporation of peroxidase into vesicles of physiologically active receptor terminals reflects a mechanism for the retrieval of vesicle membrane after exocytosis.

Role of Mitochondrial Dysfunction in the Ca2+-Induced Decline of Transmitter Release at K+-Depolarized Motor Neuron Terminals

1999 ◽  
Vol 81 (2) ◽  
pp. 498-506 ◽  
Author(s):  
Michelle A. Calupca ◽  
Gregory M. Hendricks ◽  
Jean C. Hardwick ◽  
Rodney L. Parsons
Keyword(s):  
Motor Neuron ◽  
Mitochondrial Dysfunction ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Prolonged Exposure ◽  
Nerve Terminals ◽  
Atp Production ◽  
Neuron Terminals ◽  
Nerve Muscle

Role of mitochondrial dysfunction in the Ca2+-induced decline of transmitter release at K+-depolarized motor neuron terminals. The present study tested whether a Ca2+-induced disruption of mitochondrial function was responsible for the decline in miniature endplate current (MEPC) frequency that occurs with nerve-muscle preparations maintained in a 35 mM potassium propionate (35 mM KP) solution containing elevated calcium. When the 35 mM KP contained control Ca2+(1 mM), the MEPC frequency increased and remained elevated for many hours, and the mitochondria within twitch motor neuron terminals were similar in appearance to those in unstimulated terminals. All nerve terminals accumulated FM1–43 when the dye was present for the final 6 min of a 300-min exposure to 35 mM KP with control Ca2+. In contrast, when Ca2+ was increased to 3.6 mM in the 35 mM KP solution, the MEPC frequency initially reached frequencies >350 s− 1 but then gradually fell approaching frequencies <50 s−1. A progressive swelling and eventual distortion of mitochondria within the twitch motor neuron terminals occurred during prolonged exposure to 35 mM KP with elevated Ca2+. After ∼300 min in 35 mM KP with elevated Ca2+, only 58% of the twitch terminals accumulated FM1–43. The decline in MEPC frequency in 35 mM KP with elevated Ca2+ was less when 15 mM glucose was present or when preparations were pretreated with 10 μM oligomycin and then bathed in the 35 mM KP with glucose. When glucose was present, with or without oligomycin pretreatment, a greater percentage of twitch terminals accumulated FM1–43. However, the mitochondria in these preparations were still greatly swollen and distorted. We propose that prolonged depolarization of twitch motor neuron terminals by 35 mM KP with elevated Ca2+ produced a Ca2+-induced decrease in mitochondrial ATP production. Under these conditions, the cytosolic ATP/ADP ratio was decreased thereby compromising both transmitter release and refilling of recycled synaptic vesicles. The addition of glucose stimulated glycolysis which contributed to the maintenance of required ATP levels.

Real-time measurement of transmitter release from single synaptic vesicles

Nature ◽  
1995 ◽  
Vol 377 (6544) ◽  
pp. 62-65 ◽  
Author(s):  
Dieter Bruns ◽  
Reinhard Jahn
Keyword(s):  
Real Time ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Time Measurement ◽  
Real Time Measurement

scholarly journals Primary and secondary motoneurons use different calcium channel types to control escape and swimming behaviors in zebrafish

2020 ◽  
Author(s):  
Hua Wen ◽  
Kazumi Eckenstein ◽  
Vivien Weihrauch ◽  
Christian Stigloher ◽  
Paul Brehm
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Muscle Cell ◽  
Transmitter Release ◽  
Escape Response ◽  
Quantal Content ◽  
Release Probability ◽  
High Release ◽  
Postsynaptic Cell ◽  
Rhythmic Contractions

AbstractThe escape response and rhythmic swimming in zebrafish are distinct behaviors mediated by two functionally distinct motoneuron (Mn) types. The primary (1°Mn) type depresses, has a large quantal content (Qc), and a high release probability (Pr). Conversely, the secondary (2°Mn) type facilitates and has low and variable Qc and Pr. This functional duality matches well the distinct associated behaviors, with the 1°Mn providing the strong, singular C-bend initiating escape and the 2°Mn confers weaker, rhythmic contractions. Contributing to these functional distinctions is our identification of P/Q type calcium channels mediating transmitter release in 1°Mns and N type channels in 2°Mns. Remarkably, despite these functional and behavioral distinctions, all ~15 individual synapses on each muscle cell are shared by a 1°Mn bouton and at least one 2°Mn bouton. This novel blueprint of synaptic sharing provides an efficient way of controlling two different behaviors at the level of a single postsynaptic cell.

Synaptic interactions between mammalian central neurons in cell culture. II. Quantal Analysis of EPSPs

1983 ◽  
Vol 49 (6) ◽  
pp. 1442-1458 ◽  
Author(s):  
P. G. Nelson ◽  
K. C. Marshall ◽  
R. Y. Pun ◽  
C. N. Christian ◽  
W. H. Sheriff ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Culture Medium ◽  
Ion Concentration ◽  
Release Mechanism ◽  
Drg Neurons ◽  
Release Process ◽  
Central Neurons ◽  
Synaptic Interactions ◽  
Presynaptic Release ◽  
The Relationship

The presynaptic release mechanism involved in excitatory synaptic connections between neurons in cell cultures of fetal mouse spinal cord were studied by statistical analysis of intracellularly recorded postsynaptic responses. Quantal parameters were determined for the EPSPs evoked in spinal cord (SC) neurons by stimulation of either other SC or dorsal root ganglion (DRG) neurons. Transmitter release was manipulated by varying the Ca2+ and Mg2+ content of the culture medium. The release process was represented better by binomial than by Poisson statistics. A method was derived for obtaining the probability of release and the number of release elements. The quantal content and the number of release elements were substantially higher for the SC-SC connection than for the DRG-SC connection. This was partially compensated for by a larger quantal amplitude for the DRG-SC connection. There was some indication that the probability of release was higher for the SC-SC connection. The relationship between transmitter output and effective external Ca2+ ion concentration was approximately linear.

Partial Uncoupling of Neurotransmitter Release From [Ca2+]i by Membrane Hyperpolarization

1999 ◽  
Vol 81 (6) ◽  
pp. 3044-3053 ◽  
Author(s):  
R. Ravin ◽  
H. Parnas ◽  
M. E. Spira ◽  
I. Parnas
Keyword(s):  
Membrane Potential ◽  
Neurotransmitter Release ◽  
Quantal Content ◽  
Presynaptic Membrane ◽  
Release Process ◽  
Membrane Hyperpolarization ◽  
Quantal Release ◽  
Asynchronous Release ◽  
Frequency Of Stimulation ◽  
Different Levels

Partial uncoupling of neurotransmitter release from [Ca2+]i by membrane hyperpolarization. The dependence of evoked and asynchronous release on intracellular calcium ([Ca2+]i) and presynaptic membrane potential was examined in single-release boutons of the crayfish opener neuromuscular junction. When a single bouton was depolarized by a train of pulses, [Ca2+]iincreased to different levels according to the frequency of stimulation. Concomitant measurements of evoked release and asynchronous release, from the same bouton, showed that both increased in a sigmoidal manner as a function of [Ca2+]i. When each of the depolarizing pulses was immediately followed by a hyperpolarizing pulse, [Ca2+]i was elevated to a lesser degree than in the control experiments, and the rate of asynchronous release and the quantal content were reduced; most importantly, evoked quantal release terminated sooner. The diminution of neurotransmitter release by the hyperpolarizing postpulse (HPP) could not be entirely accounted for by the reduction in [Ca2+]i. The experimental results are consistent with the hypothesis that the HPP reduces the sensitivity of the release machinery to [Ca2+]i, thereby not only reducing the quantal content but also terminating the quantal release process sooner.

Structural and functional changes of frog neuromuscular junctions in high calcium solutions

1971 ◽  
Vol 178 (1053) ◽  
pp. 407-415 ◽  
Keyword(s):  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Secretory Response ◽  
Spontaneous Release ◽  
Functional Changes ◽  
High Calcium ◽  
Release Of Acetylcholine ◽  
Evoked Transmitter Release

When frog muscles are exposed for several hours to a solution of isotonic calcium chloride, the secretory response of the motor nerve terminals to imposed depolarization ultimately fails and the rate of spontaneous release of acetylcholine also declines towards zero. The failure of depolarization-evoked transmitter release is irreversible while spontaneous release reappears, though in highly abnormal fashion, when the muscle is returned to a normal ionic medium. Examination of motor end-plates, during various stages of calcium treatment, shows that there is gradual intra-axonal agglutination of synaptic vesicles which is only very incompletely reversible. This effect is presumably the consequence of gradual entry and intracellular accumulation of calcium ions. Analogous treatment with isotonic magnesium, while resulting in immediate loss of evoked transmitter release, does not lead to progressive agglutination of synaptic vesicles, nor to irreversible impairment of the secretory response of the nerve terminal. The possible relations between structural and functional changes during calcium and magnesium treatment are discussed.

scholarly journals Analysis of Multiquantal Transmitter Release From Single Cultured Cortical Neuron Terminals

1999 ◽  
Vol 81 (4) ◽  
pp. 1810-1817 ◽  
Author(s):  
Oliver Prange ◽  
Timothy H. Murphy
Keyword(s):  
Cortical Neuron ◽  
Cortical Neurons ◽  
Transmitter Release ◽  
Primary Cultures ◽  
Three Dimensional ◽  
Variable Number ◽  
Release Process ◽  
Release Probability ◽  
Synaptic Terminals ◽  
Neuron Terminals

Analysis of multiquantal transmitter release from single cultured cortical neuron terminals. Application of single synapse recording methods indicates that the amplitude of postsynaptic responses of single CNS synapses can vary greatly among repeated stimuli. To determine whether this observation could be attributed to synapses releasing a variable number of transmitter quanta, we assessed the prevalence of multiquantal transmitter release in primary cultures of cortical neurons with the action potential (AP)-dependent presynaptic turnover of the styryl dye FM1–43 ( Betz and Bewick 1992 , 1993 ; Betz et al. 1996 ). It was assumed that if a high proportion of vesicles within a terminal were loaded with FM1–43 the amount of dye released per stimulus would be proportional to the number of quanta released and/or the probability of release at a terminal. To rule out differences in the amount of release (between terminals) caused by release probability or incomplete loading of terminals, conditions were chosen to maximize both release probability and terminal loading. Three-dimensional reconstruction of terminals was employed to ensure that bouton fluorescence was accurately measured. Analysis of the relationship between the loading of terminals and release indicated that presumed larger terminals (>FM1–43 uptake) release a greater amount of dye per stimulus than smaller terminals, suggesting multiquantal release. The distribution of release amounts across terminals was significantly skewed toward higher values, with 13–17% of synaptic terminals apparently releasing multiple quanta per AP. In conclusion, our data suggest that most synaptic terminals release a relatively constant amount of transmitter per stimulus; however, a subset of terminals releases amounts of FM1–43 that are greater than that expected from a unimodal release process.

scholarly journals Botulinum Neurotoxin a Blocks Synaptic Vesicle Exocytosis but Not Endocytosis at the Nerve Terminal

1999 ◽  
Vol 147 (6) ◽  
pp. 1249-1260 ◽  
Author(s):  
Elaine A. Neale ◽  
Linda M. Bowers ◽  
Min Jia ◽  
Karen E. Bateman ◽  
Lura C. Williamson
Keyword(s):  
Synaptic Vesicle ◽  
Nerve Terminal ◽  
Neurotransmitter Release ◽  
Synaptic Vesicles ◽  
Botulinum Neurotoxin ◽  
Vesicle Membrane ◽  
Botulinum Neurotoxin A ◽  
Synaptic Vesicle Exocytosis ◽  
Vesicle Exocytosis ◽  
Botulinum Neurotoxins

The supply of synaptic vesicles in the nerve terminal is maintained by a temporally linked balance of exo- and endocytosis. Tetanus and botulinum neurotoxins block neurotransmitter release by the enzymatic cleavage of proteins identified as critical for synaptic vesicle exocytosis. We show here that botulinum neurotoxin A is unique in that the toxin-induced block in exocytosis does not arrest vesicle membrane endocytosis. In the murine spinal cord, cell cultures exposed to botulinum neurotoxin A, neither K+-evoked neurotransmitter release nor synaptic currents can be detected, twice the ordinary number of synaptic vesicles are docked at the synaptic active zone, and its protein substrate is cleaved, which is similar to observations with tetanus and other botulinal neurotoxins. In marked contrast, K+ depolarization, in the presence of Ca2+, triggers the endocytosis of the vesicle membrane in botulinum neurotoxin A–blocked cultures as evidenced by FM1-43 staining of synaptic terminals and uptake of HRP into synaptic vesicles. These experiments are the first demonstration that botulinum neurotoxin A uncouples vesicle exo- from endocytosis, and provide evidence that Ca2+ is required for synaptic vesicle membrane retrieval.

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