Resting Calcium Levels and Evoked Release at the Neuromuscular Junction

Kloot, William Van der; Cohen, Ira S.; Barton, Stuart B.

doi:10.1007/978-1-4613-2307-5_11

Cited by 3 publications

(2 citation statements)

References 37 publications

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“…MEPP frequency, f, appears to be a function of a power, II, of the intracellular [Ca" I,,, , f = [Ca2+]inn (Dodge and Rahamimoff, 1967;Van der Kloot, 1978;Steinbach and Stevens, 1976). The minimum value of n appears to be 4 (Parnas and Segal, 1981;Van der Kloot, 1983: Cohen andVan der Kloot, 1985;Van der Kloot, Cohen, and Barton. 1986).…”

Section: How Much Does [Ca2+] Rise?mentioning

confidence: 96%

Down‐regulation of quantal size at frog neuromuscular junctions: Possible roles for elevated intracellular calcium and for protein kinase C

Kloot

1991

J. Neurobiol.

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Previous work showed that quantal size can be at least doubled at the frog neuromuscular junction by pretreatment with hormones or hypertonic solutions, primarily by the release of more acetylcholine (ACh) per quantum. Once increased, quantal size slowly declined over hours. Quantal size was measured from miniature end-plate potentials (MEPPs) or currents (MEPCs). In the present experiments, preparations in which quantal size had been increased were exposed to 17-25 mM [K+], quantal size decreased within minutes. Release of comparable numbers of quanta by nerve stimulation did not decrease size. K(+)-solutions did not decrease size if Ca2+ was omitted or replaced with Sr2+. The phosphokinase C (PKC) activators phorbol 12,13-diacetate (PDA) and 1-oleoyl-2-acetyl-rac-glycerol (OAG) also decreased quantal size within minutes when applied in a hypertonic solution that increased the rate of spontaneous release. Phorbol 12,13-dideconate, which does not activate PKC, did not decrease quantal size. The size decrease triggered by K(+)-solutions or PKC activators was blocked by 100 microM 1-(5-isoquinolinyl-sulfonyl)-2-methyl-piperazine (H7), a protein kinase inhibitor. Apparently, increasing [K+] elevated intracellular [Ca2+], which activates PKC, and which leads to the down-regulation of quantal size. During the period in which size is decreasing, there appears to be large and normal subpopulations of MEPP sizes, with normal gradually replacing large. This suggests that large quanta are formed by adding additional ACh to preformed quanta shortly before they are available for release.

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Section: How Much Does [Ca2+] Rise?mentioning

confidence: 96%

Down‐regulation of quantal size at frog neuromuscular junctions: Possible roles for elevated intracellular calcium and for protein kinase C

Kloot

1991

J. Neurobiol.

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“…Hypertonicity stimulates quantal secretion of ACh independently of extracellular Ca2+, presumably by reducing the volume of the terminal and thereby increasing intracellular Ca2+ concentration (Shimoni et al 1977;Van der Kloot, Cohen & Barton, 1986). Fusions still predominate near the active zones, possibly due to a locally higher concentration either of vesicles or of sites for exocytosis.…”

Section: Intracellular Recordings During Chemical Fixationmentioning

confidence: 99%

The effect of potassium on exocytosis of transmitter at the frog neuromuscular junction.

Ceccarelli

Fesce

Grohovaz

et al. 1988

The Journal of Physiology

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SUMMARY1. Electrophysiology and morphology have been combined to investigate the time course of the exocytosis of quanta of neurotransmitter induced by elevated concentrations of K+ at the frog neuromuscular junction.2. Replicas of freeze-fractured resting nerve terminals fixed in the presence of 20 mM-K+ showed images of fusion of synaptic vesicles with the presynaptic axolemma which were closely associated with the active zones. After 1 min in 20 mm-K+ fusions appeared also outside the active zones, and by 5 min they became uniformly distributed over the presynaptic membrane.3. The average total density of fusions was not significantly different at the various times examined since it decreased at the active zones while it increased over the rest of the membrane.4. Resting terminals fixed in 20 mM-K+ released 33000-45000 quanta after the addition of fixative; terminals stimulated by 20 mM-K+ for 1-5 min released 50000-100000 quanta during fixation. The fixative potentiated K+-induced transmitter release.5. Fusions were uniformly distributed in terminals pre-incubated for 5 min in 20 mM-K+ without added Ca2+, stimulated by adding Ca2`for 30 s, and then fixed. Conversely, after 5 min stimulation in hypertonic Ringer solution fusions remained predominantly located near the active zones. A similar distribution was observed after 15 min stimulation by a lower concentration of K+ (15 mM).6. At all concentrations of K+ tested (10, 15, 20, 25 mM) miniature end-plate potential (MEPP) rate attained a steady-state value within 10-15 min. Values from a single junction were generally lower at higher concentrations of K+, which indicates partial inactivation of the secretion-recycling process.7. The data indicate that K+ initially activates exocytosis at the active zones.Subsequently, ectopic exocytosis is activated while sites at the active zones appear to undergo partial inactivation. These phenomena are not related to the intensity or to the amount of previous secretion.

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Adenosine Modulates Inspiratory Neurons and the Respiratory Pattern in the Brainstem of Neonatal Rats

1997

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The role of adenosine in the modulation of respiration-related neurons was examined using an in vitro brainstem-spinal cord preparation from neonatal rats (0-4 d old). Respiratory activity was recorded from the C4 or C5 ventral roots by suction electrodes and from inspiratory related neurons (I neurons) in the rostral ventrolateral medulla by microelectrodes. The following substances were added to the preparation superfusate, and their effect was evaluated: the adenosine A1 receptor agonist N6-(2-phenylisopropyl)adenosine, R(-)isomer (R-PIA), the adenosine uptake blocker dipyridamole, the adenosine receptor antagonist theophylline, and the specific A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). R-PIA and dipyridamole decreased the activity of I neurons and the C4 respiratory burst rate. Furthermore, these compounds induced a significantly more irregular respiratory rate in three-quarters of preparations from the youngest animals (<48 h old) compared with that of controls. Theophylline or DPCPX reversed the effects of both R-PIA and dipyridamole on respiratory rate, regularity of respiratory rate, inspiratory time, amplitude, and intra-burst frequency of I neurons. Thus, adenosine depresses both the I neurons in the rostral ventrolateral medulla and the respiratory motor output. This depression of I neurons and respiratory rate can be abolished by theophylline primarily through a blockade of medullary adenosine A1 receptors. An age-dependent correlation of the effects of R-PIA and dipyridamole, with a more pronounced decrease in respiratory activity in preparations from younger animals, indicates that adenosinergic modulation of medullary respiration-related neurons changes during the first days of postnatal life.

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Resting Calcium Levels and Evoked Release at the Neuromuscular Junction

Cited by 3 publications

References 37 publications

Down‐regulation of quantal size at frog neuromuscular junctions: Possible roles for elevated intracellular calcium and for protein kinase C

Down‐regulation of quantal size at frog neuromuscular junctions: Possible roles for elevated intracellular calcium and for protein kinase C

The effect of potassium on exocytosis of transmitter at the frog neuromuscular junction.

Adenosine Modulates Inspiratory Neurons and the Respiratory Pattern in the Brainstem of Neonatal Rats

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