Acute stress is not acute: sustained enhancement of glutamate release after acute stress involves readily releasable pool size and synapsin I activation

2016 ◽  
Vol 22 (9) ◽  
pp. 1226-1227 ◽  
Author(s):  
L Musazzi ◽  
P Tornese ◽  
N Sala ◽  
M Popoli
Keyword(s):  
Acute Stress ◽  
Glutamate Release ◽  
Pool Size ◽  
Synapsin I ◽  
Releasable Pool ◽  
Readily Releasable Pool

VARIATION IN SIZE OF THE 'READILY RELEASABLE POOL' OF LUTEINIZING HORMONE DURING THE OESTROUS CYCLE OF THE RAT

1979 ◽  
Vol 83 (1) ◽  
pp. 53-59 ◽  
Author(s):  
A. J.-M. C. PICKERING ◽  
G. FINK
Keyword(s):  
Luteinizing Hormone ◽  
Fold Increase ◽  
Pool Size ◽  
Oestrous Cycle ◽  
Apparent Increase ◽  
Storage Pool ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Significant Change

SUMMARY The size of the 'readily releasable pool' of luteinizing hormone at various times of the oestrous cycle has been determined by injecting a supramaximal dose of luteinizing hormone releasing factor (LH-RF) i.v. into rats anaesthetized with sodium pentobarbitone. In an attempt to block replenishment of the 'pool' during release, cycloheximide was administered 30 min before LH-RF. A 20-fold increase in pool size occurred between the morning of dioestrus and the evening of pro-oestrus in the absence of any significant change in total pituitary content of LH. This suggests that increased responsiveness may be brought about by a change in the receptor-release apparatus and/or a transfer of LH from a 'storage pool' which leads to an apparent increase in the proportion of LH available for release.

scholarly journals Munc18-1 expression levels control synapse recovery by regulating readily releasable pool size

2006 ◽  
Vol 103 (48) ◽  
pp. 18332-18337 ◽  
Author(s):  
R. F. G. Toonen ◽  
K. Wierda ◽  
M. S. Sons ◽  
H. de Wit ◽  
L. N. Cornelisse ◽  
...  
Keyword(s):  
Pool Size ◽  
Expression Levels ◽  
Releasable Pool ◽  
Readily Releasable Pool

scholarly journals Huntingtin-associated protein 1 regulates exocytosis, vesicle docking, readily releasable pool size and fusion pore stability in mouse chromaffin cells

2014 ◽  
Vol 592 (7) ◽  
pp. 1505-1518 ◽  
Author(s):  
Kimberly D. Mackenzie ◽  
Michael D. Duffield ◽  
Heshan Peiris ◽  
Lucy Phillips ◽  
Mark P. Zanin ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Pool Size ◽  
Fusion Pore ◽  
Vesicle Docking ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Pore Stability

scholarly journals The mammalian rod synaptic ribbon is essential for Cav channel facilitation and ultrafast fusion of the readily releasable pool of vesicles

2020 ◽  
Author(s):  
Chad Paul Grabner ◽  
Tobias Moser
Keyword(s):  
Visual Information ◽  
Release Kinetics ◽  
Glutamate Release ◽  
Wild Type ◽  
Synaptic Ribbon ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Ribbon Synapses ◽  
Channel Opening ◽  
Intracellular Ca

AbstractRod photoreceptors (PRs) use ribbon synapses to transmit visual information. To signal ‘no light detected’ they release glutamate continually to activate post-synaptic receptors, and when light is detected glutamate release pauses. How a rod’s individual ribbon enables this process was studied here by recording evoked changes in whole-cell membrane capacitance from wild type and ribbonless (RIBEYE-ko) rods. Wild type rods created a readily releasable pool (RRP) of 92 synaptic vesicles (SVs) that emptied as a single kinetic phase with a τ < 0.4 msec. Lowering intracellular Ca2+-buffering accelerated Cav channel opening and facilitated release kinetics, but RRP size was unaltered. In contrast, ribbonless rods created an RRP of 24 SVs, and lacked Cav channel facilitation; however, Ca2+ channel-release coupling remained tight. The release deficits caused a sharp attenuation of rod-driven light responses measured from RIBEYE-ko mice. We conclude that the synaptic ribbon facilitates Ca2+-influx and establishes a large RRP of SVs.

Inhibition of presynaptic Na+/K+-ATPase reduces readily releasable pool size at the avian end-bulb of Held synapse

2012 ◽  
Vol 72 (2) ◽  
pp. 117-128 ◽  
Author(s):  
Akiyuki Taruno ◽  
Harunori Ohmori ◽  
Hiroshi Kuba
Keyword(s):  
Pool Size ◽  
Releasable Pool ◽  
Readily Releasable Pool

scholarly journals Lack of Synapsin I Reduces the Readily Releasable Pool of Synaptic Vesicles at Central Inhibitory Synapses

2007 ◽  
Vol 27 (49) ◽  
pp. 13520-13531 ◽  
Author(s):  
P. Baldelli ◽  
A. Fassio ◽  
F. Valtorta ◽  
F. Benfenati
Keyword(s):  
Synaptic Vesicles ◽  
Inhibitory Synapses ◽  
Synapsin I ◽  
Releasable Pool ◽  
Readily Releasable Pool

Presynaptic Na+/K+ ATPase activity maintains readily releasable pool size at the avian end-bulb of Held synapse

2009 ◽  
Vol 65 ◽  
pp. S80
Author(s):  
Akiyuki Taruno ◽  
Hiroshi Kuba ◽  
Harunori Ohmori
Keyword(s):  
Atpase Activity ◽  
Pool Size ◽  
Releasable Pool ◽  
Readily Releasable Pool

scholarly journals Synapsin I-associated Phosphatidylinositol 3-Kinase Mediates Synaptic Vesicle Delivery to the Readily Releasable Pool

2003 ◽  
Vol 278 (31) ◽  
pp. 29065-29071 ◽  
Author(s):  
Michael A. Cousin ◽  
Chandra S. Malladi ◽  
Timothy C. Tan ◽  
Clarke R. Raymond ◽  
Karen J. Smillie ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Synapsin I ◽  
Phosphatidylinositol 3 Kinase ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Phosphatidylinositol 3

scholarly journals Synapsins I and II Are Not Required for Insulin Secretion from Mouse Pancreatic β-cells

Endocrinology ◽  
2012 ◽  
Vol 153 (5) ◽  
pp. 2112-2119 ◽  
Author(s):  
Anna Wendt ◽  
Dina Speidel ◽  
Anders Danielsson ◽  
Jonathan L. S. Esguerra ◽  
Inger Lise Bogen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Synapsin I ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Double Knockout ◽  
Knock Out ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Voltage Dependent ◽  
Glucose Stimulated Insulin Secretion

Synapsins are a family of phosphoproteins that modulate the release of neurotransmitters from synaptic vesicles. The release of insulin from pancreatic β-cells has also been suggested to be regulated by synapsins. In this study, we have utilized a knock out mouse model with general disruptions of the synapsin I and II genes [synapsin double knockout (DKO)]. Stimulation with 20 mm glucose increased insulin secretion 9-fold in both wild-type (WT) and synapsin DKO islets, whereas secretion in the presence of 70 mm K+ and 1 mm glucose was significantly enhanced in the synapsin DKO mice compared to WT. Exocytosis in single β-cells was investigated using patch clamp. The exocytotic response, measured by capacitance measurements and elicited by a depolarization protocol designed to visualize exocytosis of vesicles from the readily releasable pool and from the reserve pool, was of the same size in synapsin DKO and WT β-cells. The increase in membrane capacitance corresponding to readily releasable pool was approximately 50fF in both genotypes. We next investigated the voltage-dependent Ca2+ influx. In both WT and synapsin DKO β-cells the Ca2+ current peaked at 0 mV and measured peak current (Ip) and net charge (Q) were of similar magnitude. Finally, ultrastructural data showed no variation in total number of granules (Nv) or number of docked granules (Ns) between the β-cells from synapsin DKO mice and WT control. We conclude that neither synapsin I nor synapsin II are directly involved in the regulation of glucose-stimulated insulin secretion and Ca2-dependent exocytosis in mouse pancreatic β-cells.

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