scholarly journals All roads lead to presynaptic calcium channel inhibition by the ghrelin receptor: Separate agonist-dependent and -independent signaling pathways

2015 ◽  
Vol 146 (3) ◽  
pp. 201-204 ◽  
Author(s):  
Norbert Weiss ◽  
Gerald W. Zamponi
2014 ◽  
Vol 34 (23) ◽  
pp. 7958-7963 ◽  
Author(s):  
G. G. Szabo ◽  
N. Lenkey ◽  
N. Holderith ◽  
T. Andrasi ◽  
Z. Nusser ◽  
...  

2019 ◽  
Vol 123 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Yuko Koyanagi ◽  
Christina L. Torturo ◽  
Daniel C. Cook ◽  
Zhenyu Zhou ◽  
Hugh C. Hemmings

2009 ◽  
Vol 23 (4) ◽  
pp. 427-438 ◽  
Author(s):  
Camila Squarzoni Dale ◽  
Christophe Altier ◽  
Nicolas Cenac ◽  
Renata Giorgi ◽  
Maria Aparecida Juliano ◽  
...  

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Michael A Gaviño ◽  
Kevin J Ford ◽  
Santiago Archila ◽  
Graeme W Davis

Homeostatic signaling stabilizes synaptic transmission at the neuromuscular junction (NMJ) of Drosophila, mice, and human. It is believed that homeostatic signaling at the NMJ is bi-directional and considerable progress has been made identifying mechanisms underlying the homeostatic potentiation of neurotransmitter release. However, very little is understood mechanistically about the opposing process, homeostatic depression, and how bi-directional plasticity is achieved. Here, we show that homeostatic potentiation and depression can be simultaneously induced, demonstrating true bi-directional plasticity. Next, we show that mutations that block homeostatic potentiation do not alter homeostatic depression, demonstrating that these are genetically separable processes. Finally, we show that homeostatic depression is achieved by decreased presynaptic calcium channel abundance and calcium influx, changes that are independent of the presynaptic action potential waveform. Thus, we identify a novel mechanism of homeostatic synaptic plasticity and propose a model that can account for the observed bi-directional, homeostatic control of presynaptic neurotransmitter release.


2020 ◽  
Vol 122 (7) ◽  
pp. 1023-1036 ◽  
Author(s):  
Karol Granados ◽  
Laura Hüser ◽  
Aniello Federico ◽  
Sachindra Sachindra ◽  
Gretchen Wolff ◽  
...  

2017 ◽  
Vol 16 (9) ◽  
pp. 2051
Author(s):  
Zhao Jin ◽  
Huisheng Wu ◽  
Chaoliang Tang ◽  
Jianjuan Ke ◽  
Yanlin Wang

2003 ◽  
Vol 278 (23) ◽  
pp. 21178-21187 ◽  
Author(s):  
J. David Spafford ◽  
Lina Chen ◽  
Zhong-Ping Feng ◽  
August B. Smit ◽  
Gerald W. Zamponi

2019 ◽  
Vol 20 (10) ◽  
pp. 2480 ◽  
Author(s):  
An Buckinx ◽  
Yana Van Den Herrewegen ◽  
Anouk Pierre ◽  
Eleonora Cottone ◽  
Khoubaib Ben Haj Salah ◽  
...  

The ghrelin system has received substantial recognition as a potential target for novel anti-seizure drugs. Ghrelin receptor (ghrelin-R) signaling is complex, involving Gαq/11, Gαi/o, Gα12/13, and β-arrestin pathways. In this study, we aimed to deepen our understanding regarding signaling pathways downstream the ghrelin-R responsible for mediating anticonvulsive effects in a kindling model. Mice were administered the proconvulsive dopamine 1 receptor-agonist, SKF81297, to gradually induce a kindled state. Prior to every SKF81297 injection, mice were treated with a ghrelin-R full agonist (JMV-1843), a Gαq and Gα12 biased ligand unable to recruit β-arrestin (YIL781), a ghrelin-R antagonist (JMV-2959), or saline. Mice treated with JMV-1843 had fewer and less severe seizures compared to saline-treated controls, while mice treated with YIL781 experienced longer and more severe seizures. JMV-2959 treatment did not lead to differences in seizure severity and number. Altogether, these results indicate that the Gαq or Gα12 signaling pathways are not responsible for mediating JMV-1843′s anticonvulsive effects and suggest a possible involvement of β-arrestin signaling in the anticonvulsive effects mediated by ghrelin-R modulation.


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