Synapsins I and II Are Not Required for Insulin Secretion from Mouse Pancreatic beta-cells
Wendt, Anna LU ; Speidel, Dina LU ; Danielsson, Anders LU ; Esguerra, Jonathan L. S. ; Bogen, Inger Lise ; Walaas, S. Ivar ; Salehi, S Albert LU
and Eliasson, Lena
LU
(2012)
In Endocrinology
153(5).
p.2112-2119
- Abstract
- Synapsins are a family of phosphoproteins that modulate the release of neurotransmitters from synaptic vesicles. The release of insulin from pancreatic beta-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 1mM glucose was significantly enhanced in the synapsin DKO mice compared to WT. Exocytosis in single beta-cells was investigated using patch clamp. The exocytotic response, measured by capacitance measurements and elicited... (More)
- Synapsins are a family of phosphoproteins that modulate the release of neurotransmitters from synaptic vesicles. The release of insulin from pancreatic beta-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 1mM glucose was significantly enhanced in the synapsin DKO mice compared to WT. Exocytosis in single beta-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 beta-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 beta-cells the Ca2+ current peaked at 0 mV and measured peak current (I-p) and net charge (Q) were of similar magnitude. Finally, ultrastructural data showed no variation in total number of granules (N-v) or number of docked granules (N-s) between the beta-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 Ca-2-dependent exocytosis in mouse pancreatic beta-cells. (Endocrinology 153: 2112-2119, 2012) (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2812998
- author
- Wendt, Anna
LU
; Speidel, Dina
LU
; Danielsson, Anders
LU
; Esguerra, Jonathan L. S.
; Bogen, Inger Lise
; Walaas, S. Ivar
; Salehi, S Albert
LU
and Eliasson, Lena
LU
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Endocrinology
- volume
- 153
- issue
- 5
- pages
- 2112 - 2119
- publisher
- Oxford University Press
- external identifiers
-
- wos:000303860700011
- pmid:22334712
- scopus:84860351783
- pmid:22334712
- ISSN
- 0013-7227
- DOI
- 10.1210/en.2011-1702
- language
- English
- LU publication?
- yes
- id
- 61fb0034-0166-402b-83d4-e320346e614e (old id 2812998)
- date added to LUP
- 2016-04-01 10:12:49
- date last changed
- 2022-02-17 07:48:16
@article{61fb0034-0166-402b-83d4-e320346e614e,
abstract = {{Synapsins are a family of phosphoproteins that modulate the release of neurotransmitters from synaptic vesicles. The release of insulin from pancreatic beta-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 1mM glucose was significantly enhanced in the synapsin DKO mice compared to WT. Exocytosis in single beta-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 beta-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 beta-cells the Ca2+ current peaked at 0 mV and measured peak current (I-p) and net charge (Q) were of similar magnitude. Finally, ultrastructural data showed no variation in total number of granules (N-v) or number of docked granules (N-s) between the beta-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 Ca-2-dependent exocytosis in mouse pancreatic beta-cells. (Endocrinology 153: 2112-2119, 2012)}},
author = {{Wendt, Anna and Speidel, Dina and Danielsson, Anders and Esguerra, Jonathan L. S. and Bogen, Inger Lise and Walaas, S. Ivar and Salehi, S Albert and Eliasson, Lena}},
issn = {{0013-7227}},
language = {{eng}},
number = {{5}},
pages = {{2112--2119}},
publisher = {{Oxford University Press}},
series = {{Endocrinology}},
title = {{Synapsins I and II Are Not Required for Insulin Secretion from Mouse Pancreatic beta-cells}},
url = {{https://lup.lub.lu.se/search/files/1657840/3052941.pdf}},
doi = {{10.1210/en.2011-1702}},
volume = {{153}},
year = {{2012}},
}