Voltage‐induced Ca 2+ release by ryanodine receptors causes neuropeptide secretion from nerve terminals

2020 ◽  
Vol 32 (4) ◽  
Author(s):  
Cristina Velázquez‐Marrero ◽  
Edward E. Custer ◽  
Héctor Marrero ◽  
Sonia Ortiz‐Miranda ◽  
José R. Lemos
Keyword(s):  
Ryanodine Receptors ◽  
Nerve Terminals ◽  
Neuropeptide Secretion

scholarly journals Suppression of Ca2+ syntillas increases spontaneous exocytosis in mouse adrenal chromaffin cells

2009 ◽  
Vol 134 (4) ◽  
pp. 267-280 ◽  
Author(s):  
Jason J. Lefkowitz ◽  
Kevin E. Fogarty ◽  
Lawrence M. Lifshitz ◽  
Karl D. Bellve ◽  
Richard A. Tuft ◽  
...  
Keyword(s):  
Simple Model ◽  
Chromaffin Cells ◽  
Ryanodine Receptors ◽  
Nerve Terminals ◽  
Adrenal Chromaffin Cells ◽  
Central Concept ◽  
Voltage Gated ◽  
Adrenal Chromaffin ◽  
Synaptic Structures ◽  
Ca2 Channels

A central concept in the physiology of neurosecretion is that a rise in cytosolic [Ca2+] in the vicinity of plasmalemmal Ca2+ channels due to Ca2+ influx elicits exocytosis. Here, we examine the effect on spontaneous exocytosis of a rise in focal cytosolic [Ca2+] in the vicinity of ryanodine receptors (RYRs) due to release from internal stores in the form of Ca2+ syntillas. Ca2+ syntillas are focal cytosolic transients mediated by RYRs, which we first found in hypothalamic magnocellular neuronal terminals. (scintilla, Latin for spark; found in nerve terminals, normally synaptic structures.) We have also observed Ca2+ syntillas in mouse adrenal chromaffin cells. Here, we examine the effect of Ca2+ syntillas on exocytosis in chromaffin cells. In such a study on elicited exocytosis, there are two sources of Ca2+: one due to influx from the cell exterior through voltage-gated Ca2+ channels, and that due to release from intracellular stores. To eliminate complications arising from Ca2+ influx, we have examined spontaneous exocytosis where influx is not activated. We report here that decreasing syntillas leads to an increase in spontaneous exocytosis measured amperometrically. Two independent lines of experimentation each lead to this conclusion. In one case, release from stores was blocked by ryanodine; in another, stores were partially emptied using thapsigargin plus caffeine, after which syntillas were decreased. We conclude that Ca2+ syntillas act to inhibit spontaneous exocytosis, and we propose a simple model to account quantitatively for this action of syntillas.

scholarly journals Dihydropyridine Receptors and Type 1 Ryanodine Receptors Constitute the Molecular Machinery for Voltage-Induced Ca2+ Release in Nerve Terminals

2006 ◽  
Vol 26 (29) ◽  
pp. 7565-7574 ◽  
Author(s):  
V. De Crescenzo ◽  
K. E. Fogarty ◽  
R. ZhuGe ◽  
R. A. Tuft ◽  
L. M. Lifshitz ◽  
...  
Keyword(s):  
Ryanodine Receptors ◽  
Nerve Terminals ◽  
Dihydropyridine Receptors ◽  
Molecular Machinery

Calcium dependence of the priming, activation and inactivation of ryanodine receptors in frog motor nerve terminals

2010 ◽  
Vol 32 (6) ◽  
pp. 948-962 ◽  
Author(s):  
Satoko Soga-Sakakibara ◽  
Masakazu Kubota ◽  
Sinichi Suzuki ◽  
Tenpei Akita ◽  
Kazuhiko Narita ◽  
...  
Keyword(s):  
Motor Nerve ◽  
Ryanodine Receptors ◽  
Nerve Terminals ◽  
Motor Nerve Terminals ◽  
Calcium Dependence

scholarly journals A Ca2+-induced Ca2+ Release Mechanism Involved in Asynchronous Exocytosis at Frog Motor Nerve Terminals

1998 ◽  
Vol 112 (5) ◽  
pp. 593-609 ◽  
Author(s):  
K. Narita ◽  
T. Akita ◽  
M. Osanai ◽  
T. Shirasaki ◽  
H. Kijima ◽  
...  
Keyword(s):  
Motor Nerve ◽  
Ryanodine Receptors ◽  
Pause Duration ◽  
Release Mechanism ◽  
Nerve Terminals ◽  
Presynaptic Terminals ◽  
Motor Nerve Terminals ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Ca2 Channels

The extent to which Ca2+-induced Ca2+ release (CICR) affects transmitter release is unknown. Continuous nerve stimulation (20–50 Hz) caused slow transient increases in miniature end-plate potential (MEPP) frequency (MEPP-hump) and intracellular free Ca2+ ([Ca2+]i) in presynaptic terminals (Ca2+-hump) in frog skeletal muscles over a period of minutes in a low Ca2+, high Mg2+ solution. Mn2+ quenched Indo-1 and Fura-2 fluorescence, thus indicating that stimulation was accompanied by opening of voltage-dependent Ca2+ channels. MEPP-hump depended on extracellular Ca2+ (0.05–0.2 mM) and stimulation frequency. Both the Ca2+- and MEPP-humps were blocked by 8-(N,N-diethylamino)octyl3,4,5-trimethoxybenzoate hydrochloride (TMB-8), ryanodine, and thapsigargin, but enhanced by CN−. Thus, Ca2+-hump is generated by the activation of CICR via ryanodine receptors by Ca2+ entry, producing MEPP-hump. A short interruption of tetanus (<1 min) during MEPP-hump quickly reduced MEPP frequency to a level attained under the effect of TMB-8 or thapsigargin, while resuming tetanus swiftly raised MEPP frequency to the previous or higher level. Thus, the steady/equilibrium condition balancing CICR and Ca2+ clearance occurs in nerve terminals with slow changes toward a greater activation of CICR (priming) during the rising phase of MEPP-hump and toward a smaller activation during the decay phase. A short pause applied after the end of MEPP- or Ca2+-hump affected little MEPP frequency or [Ca2+]i, but caused a quick increase (faster than MEPP- or Ca2+-hump) after the pause, whose magnitude increased with an increase in pause duration (<1 min), suggesting that Ca2+ entry-dependent inactivation, but not depriming process, explains the decay of the humps. The depriming process was seen by giving a much longer pause (>1 min). Thus, ryanodine receptors in frog motor nerve terminals are endowed with Ca2+ entry-dependent slow priming and fast inactivation mechanisms, as well as Ca2+ entry-dependent activation, and involved in asynchronous exocytosis. Physiological significance of CICR in presynaptic terminals was discussed.

Computer-Assisted Analysis of Multi-Color Confocal Microscopic Datasets: Automated Light Microscopic Discrimination of Synaptic Relationships

1996 ◽  
Vol 54 ◽  
pp. 284-285
Author(s):  
M Wessendorf ◽  
A Beuning ◽  
D Cameron ◽  
J Williams ◽  
C Knox
Keyword(s):  
Nerve Fibers ◽  
Confocal Scanning Laser Microscopy ◽  
Computer Assisted ◽  
Nerve Terminals ◽  
Neuronal Somata ◽  
Scanning Laser Microscopy ◽  
Confocal Scanning ◽  
Entire Cell ◽  
Confocal Scanning Laser ◽  
Assisted Analysis

Multi-color confocal scanning-laser microscopy (CSLM) allows examination of the relationships between neuronal somata and the nerve fibers surrounding them at sub-micron resolution in x,y, and z. Given these properties, it should be possible to use multi-color CSLM to identify relationships that might be synapses and eliminate those that are clearly too distant to be synapses. In previous studies of this type, pairs of images (e.g., red and green images for tissue stained with rhodamine and fluorescein) have been merged and examined for nerve terminals that appose a stained cell (see, for instance, Mason et al.). The above method suffers from two disadvantages, though. First, although it is possible to recognize appositions in which the varicosity abuts the cell in the x or y axes, it is more difficult to recognize them if the apposition is oriented at all in the z-axis—e.g., if the varicosity lies above or below the neuron rather than next to it. Second, using this method to identify potential appositions over an entire cell is time-consuming and tedious.

Nerve Terminals Associated with the Central Lacteal Endothelial Cells

1989 ◽  
Vol 66 (1) ◽  
pp. 57-59 ◽  
Author(s):  
Sanae ICHIKAWA ◽  
Shigeo UCHINO ◽  
Yukio HIRATA
Keyword(s):  
Endothelial Cells ◽  
Nerve Terminals
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