Axonal morphogenesis affected by docosahexaenoic acid and its ethanolamide derivative, Synaptamide.

Thursday, October 11, 2012 — Poster Session IV
2:00 p.m. – 4:00 p.m.	Natcher Conference Center, Building 45	NIAAA	NEURO/BEHAV/SENSYS-15

* FARE Award Winner

Author

• H.Y. Kim

Abstract

Docosahexaenoic acid (DHA, 22:6n-3) and its endogenous metabolite N-docosahexaenoylethanolamide (synaptamide) have been shown to promote development of hippocampal neurons by stimulating neurite outgrowth and synaptogenesis. Axonal bulbs and spheroids are formed various stressful conditions may contribute to functional impairment of neurons. In this study, we tested if DHA and synaptamide regulate structural development including spheroid formation and axonal growth. We found that average area of the spheroids stained for neurofilament H in vehicle treated neurons was significantly reduced by 48hr supplementation with 1 M DHA or 10 nM synaptamide (69% and 67% of control, respectively, P<0.001). Interestingly, non-omega-3 fatty acids, docosapentaenoic (22:5n-6) or oleic acid (18:1n-9), at 1 M concentration had no significant effect on axonal spheroid area, when compared to control (100% and 90% of control, respectively, P>0.05, non-significant). In addition, axonal length evaluated by staining with axon-specific SMI-312 antibody indicated that DHA at 1 M and synaptamide at 10 nM similarly induced 1.6-1.7 fold increase of the average axon length compared to control (P<0.0001). Based on our results we conclude that DHA and synaptamide promote axon development by reducing spheroid size and increasing average length of the axon.

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