Regulation of GFR alpha-1 and GFR alpha-2 mRNAs in rat brain by electroconvulsive seizure

Citation
Ach. Chen et al., Regulation of GFR alpha-1 and GFR alpha-2 mRNAs in rat brain by electroconvulsive seizure, SYNAPSE, 39(1), 2001, pp. 42-50
Citations number
43
Categorie Soggetti
Neurosciences & Behavoir
Journal title
SYNAPSE
ISSN journal
08874476 → ACNP
Volume
39
Issue
1
Year of publication
2001
Pages
42 - 50
Database
ISI
SICI code
0887-4476(200101)39:1<42:ROGAAG>2.0.ZU;2-L
Abstract
The influence of both acute and chronic electroconvulsive seizure (ECS) or antidepressant drug treatments on expression of mRNAs encoding glial cell l ine-derived neurotrophic factor (GDNF) and its receptors, GFR alpha -1, GFR alpha -2, and c-Ret proto-oncogene (RET) in the rat hippocampus was examin ed by in situ hybridization. Tyro hours after acute ECS, levels of GFR alph a -1 mRNA in the dentate gyrus were significantly increased. This increase peaked to nearly 3-fold at 6 h after acute ECS and returned to basal levels 24 h after treatment. Chronic (once daily for 10 days) ECS significantly i ncreased the expression of GFR alpha -1 mRNA nearly 5-fold after the last t reatment. Levels of GFR alpha -2 mRNA in the dentate gyrus were also signif icantly in creased by acute and chronic ECS, although this effect was less than that observed for GFR alpha -1. Maximum induction of GFR alpha -2 was 30% and 70% compared to sham in response to acute or chronic ECS, respectiv ely. Levels of GDNF and RET mRNAs were not significantly changed following either acute or chronic ECS treatment at the time points examined. Chronic (14 days) administration of different classes of antidepressant drugs, incl uding tranylcypromine, desipramine, or fluoxetine, did not significantly af fect the GDNF, GFR alpha -1, GFR alpha -2, or RET mRNA levels in CA1, CA3, and dentate gyrus areas of hippocampus. The results demonstrate that acute ECS increases the expression of GFR alpha -1 and GFR alpha -2 and that thes e effects are enhanced by chronic ECS. The results also imply that regulati on of the binding components of GDNF receptor complex may mediate the adapt ive responses of the GDNF system to acute and chronic stimulation. (C) 2001 Wiley-Liss, Inc.