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Induction of Neuronal Vascular Endothelial Growth Factor Expression by cAMP in the Dentate Gyrus of the Hippocampus Is Required for Antidepressant-Like Behaviors

Authors
Lee, Jeong-SikJang, Deok-JinLee, NuribalhaeKo, Hyoung-GonKim, HyoungKim, Yong-SeokKim, ByungwooSon, JuneheeKim, Sung HyunChung, HeekyoungLee, Mun-YongKim, Woon RyoungSun, WoongZhuo, MinAbel, TedKaang, Bong-KiunSon, Hyeon
Issue Date
1-7월-2009
Publisher
SOC NEUROSCIENCE
Keywords
ELEMENT-BINDING PROTEIN; NEUROTROPHIC FACTOR; RECEPTOR FUNCTION; RAT HIPPOCAMPUS; MESSENGER-RNA; IN-VITRO; NEUROGENESIS; DEPRESSION; BRAIN; VEGF
Citation
JOURNAL OF NEUROSCIENCE, v.29, no.26, pp.8493 - 8505
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF NEUROSCIENCE
Volume
29
Number
26
Start Page
8493
End Page
8505
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/119691
DOI
10.1523/JNEUROSCI.1321-09.2009
ISSN
0270-6474
Abstract
The cAMP cascade and vascular endothelial growth factor (VEGF) are critical modulators of depression. Here we have tested whether the antidepressive effect of the cAMP cascade is mediated by VEGF in the adult hippocampus. We used a conditional genetic system in which the Aplysia octopamine receptor (Ap oa(1)), a G(s)-coupled receptor, is transgenically expressed in the forebrain neurons of mice. Chronic activation of the heterologous Ap oa(1) by its natural ligand evoked antidepressant-like behaviors, accompanied by enhanced phosphorylation of cAMP response element-binding protein and transcription of VEGF in hippocampal dentate gyrus (DG) neurons. Selective knockdown of VEGF in these cells during the period of cAMP elevation inhibited the antidepressant-like behaviors. These findings reveal a molecular interaction between the cAMP cascade and VEGF expression, and the pronounced behavioral consequences of this interaction shed light on the mechanism underlying neuronal VEGF functions in antidepression.
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