Premium
Differential expression of synaptic vesicle proteins after repeated electroconvulsive seizures in rat frontal cortex and hippocampus
Author(s) -
Elfving Betina,
Bonefeld Birgit Egeskov,
Rosenberg Raben,
Wegener Gregers
Publication year - 2008
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20538
Subject(s) - synapsin , synapsin i , hippocampus , synaptotagmin 1 , neuroscience , downregulation and upregulation , electroconvulsive therapy , synaptic vesicle , synapse , neurotransmitter , synaptic plasticity , endocrinology , medicine , chemistry , psychology , receptor , central nervous system , gene , vesicle , biochemistry , cognition , membrane
Electroconvulsive therapy (ECT) remains the treatment of choice for patients with severe or drug‐resistant depressive disorders, yet the mechanism behind its efficacy and the effect on neurotransmission is essentially unknown. As synaptic vesicle proteins (SVPs) are required for vesicle fusion and neurotransmitter release, we have examined the effect of single and repeated electroconvulsive seizures (ECS), an animal model of ECT, on the expression of 14 SVPs in the rat frontal cortex and the hippocampus using quantitative real‐time polymerase chain reaction (real‐time qPCR). Only in the frontal cortex, the mRNA level of synapsin II was significantly upregulated after repeated ECS. In contrast, the mRNA levels of 6 of the 14 SVPs were significantly regulated in the hippocampus after ECS. We found that SNAP29 was upregulated and synaptotagmin III was downregulated after one single ECS in the hippocampus. Furthermore, SNAP29, synapsin I, synapsin III, VAMP2, and VAMP5 were significantly upregulated, whereas synaptotagmin III was significantly downregulated after repeated ECS in the hippocampus. We suggest that these genes are highly important in the long‐term therapeutic effect of ECS, and thus it can behypothesized that the SVPs are involved in the pathophysiology of depression. Synapse 62:662–670, 2008. © 2008 Wiley‐Liss, Inc.