October 9 - 12, 2012
Building 10 & Natcher Conference Center
- General Schedule of Events
- Opening Plenary Session
- Concurrent Symposia Sessions
- Poster Sessions
- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
- TSA Research Festival Exhibit Show
- Clinical Center Tours
- Research Festival Committees
- Past Research Festivals
Ethanol impairs synaptamide-mediated neural stem cells differentiation
| Wednesday, November 06, 2013 — Poster Session I | |||
|---|---|---|---|
4:00 p.m. – 6:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NIAAA |
NEURO-18 |
Author
- H-Y Kim
Abstract
Docosahexaenoic acid (DHA) has been shown to promote neuronal differentiation of neural stem cells (NSCs) in vivo and in vitro. N-docosahexenoyethanolamine (synaptamide), an endogenous DHA metabolite with endocannabinoid-like structure, promotes neurite growth, synaptogenesis and synaptic function. Recently, we found that synaptamide is a potent neurogenic factor for neural stem cell differentiation. In this study we demonstrate that ethanol impairs synaptamide-mediated neural stem cells differentiation. We found that chronic ethanol (50-100 mM) exposure by treating NSCs with ethanol-containing media daily for 4 days decreased the number of MAP2 and Tuj-1 positive neurons and PKA/CREB phosphorylation. We also found that cellular cAMP production, which was significantly increased by synaptamide, was decreased dose-dependently by chronic ethanol treatment. Adenylate cyclase inhibitor (SQ) inhibited synaptamide-induced cAMP production, and ethanol further decreased the cAMP level. In addition, ethanol significantly increased expression of a cAMP specific phosphodiesterase PDE4. Selective inhibition of PDE4 by rolipram enhanced cAMP production and this effect was also significant attenuated by the chronic ethanol treatment. Furthermore, treatment of NSCs with ethanol decreased GTP binding protein Gs alpha. These results suggest that chronic ethanol impaired neuronal differentiation of NSCs by affecting synaptamide-mediated G-protein coupled receptor signaling involving Gs alpha.
