Gregory J Cole
Research
The current research emphasis of Dr. Cole's laboratory is to understand the mechanisms of ethanol- and cannabinoid-induced central nervous system abnormalities in zebrafish. His longstanding research interest has been the role of the extracellular matrix in nervous system development, especially the function of the heparan sulfate proteoglycan agrin. These studies are currently focusing on elucidating the mechanisms by which agrin modulates the function of heparin-binding growth factors and morphogens, such as fibroblast growth factors (Fgfs) and sonic hedgehog (Shh), during zebrafish nervous system development. The major emphasis of the laboratory is the investigation of the role of agrin in fetal alcohol spectrum disorders (FASD) and how agrin function via Fgfs and Shh is a target of embryonal ethanol and cannabinoid exposure in zebrafish. These studies are employing genetic and molecular approaches to examine ocular, forebrain, and hindbrain development in response to ethanol exposure, and the subsequent changes in agrin, Fgf or Shh signaling. A goal of Dr. Cole's laboratory is to correlate these molecular changes, as a consequence of embryonic ethanol exposure, to behavioral changes in juvenile and adult zebrafish.
Education
B.A., Biology |
State University of New York, Plattsburgh, NY |
1976 |
Ph.D, Biological Science (Program in Neuroscience) |
Florida State University, Tallahassee, FL |
1982 |
Affiliations
Member, Program in Toxicology, Duke University
Courses
Projects
Publications
- Boa-Amponsem O, Zhang C, Burton DF, Williams KP, and Cole GJ. (2020). Ethanol and cannabinoids regulate zebrafish GABAergic neuron development and behavior in a sonic hedgehog and fibroblast growth factor dependent mechanism. Alcohol. Clin. Exp. Res. 44, 1366-1377.
- Boa-Amponsem O, Zhang C, Mukhopadhyay S, Ardrey, A, and Cole GJ. (2019). Ethanol and cannabinoids interact to alter behavior in a zebrafish fetal alcohol spectrum disorder model. Birth Defects Research 111, 775-788.
- Fish EW, Murdaugh LB, Zhang C, Boschen KE, Boa-Amponsem O, Mendoza-Romero HN, Tarpley M, Chdid L, Mukhopadhyay S, Cole GJ, Williams KP, and Parnell SE. (2019). Cannabinoids exacerbate alcohol teratogenesis by a CB1-hedgehog interaction. Scientific Reports, 9:16057 | https://doi.org/10.1038/s41598-019-52336-w.
- Zhang, C*, Boa-Amponsem, O*, and Cole, GJ. (2017). Comparison of molecular marker expression in early zebrafish brain development following chronic ethanol or morpholino treatment. Exp. Brain Res. 235, 2413-2423.
- Bailey, JM, Oliveri, AN, Zhang, C, Frazier, JM, Mackinnon, S, Cole, GJ and Levin ED (2015). Long-term behavioral impairment following acute embryonic ethanol exposure in zebrafish. Neurotoxicol. Teratol. 48, 1-8.
- Zhang, C., Frazier, J.M., Chen, H., Liu, Y., Lee, J.AA., and Cole, G.J. (2014). Molecular and morphological changes in zebrafish following transient ethanol exposure during defined developmental stages. Neurotoxicol. Teratol. 44, 70-80.
- Zhang, C., Ojiaku, P. and Cole, G.J. (2013). Forebrain and hindbrain development in zebrafish is sensitive to ethanol exposure involving agrin, Fgf and Sonic hedgehog function. Birth Defects Res. (Part A) 97, 8-27.
- Xiao, T., Robles, E., Staub, W., Gosse, N.J., Cole, G.J., and Baier, H. (2011). Assembly of lamina-specific neuronal connections by a Slit gradient anchored to type IV collagen. Cell 146, 164-176.
- Zhang, C., Turton, Q.M., MacKinnon, S., Sulik, K.K. and Cole, G.J. (2011). Agrin function associated with ocular development is a target of ethanol exposure in embryonic zebrafish. Birth Defects Res. (Part A) 91, 129-141.
- Liu, I.-H., Zhang, C., Kim, M.J. and Cole, G.J. (2008). Retina development in zebrafish requires the heparan sulfate proteoglycan agrin. Dev. Neurobiol. 68, 877-898.
Grants
9/18/–8/21
NIH R21 AA025400, P.I., “Gene-ethanol interactions in a zebrafish multi-binge FASD model," $405,079 total costs.
11/17–7/18
NIH U54 AA019765-08S1, P.I., “Mechanisms of Alcohol Pathology: A Collaborative Partnership Between NCCU & UNC," $45,542 total costs.
3/17–7/19
NIH U54 AA019765-07S1, P.I., “Mechanisms of Alcohol Pathology: A Collaborative Partnership Between NCCU & UNC," $24,687 total costs.
8/15–7/21
NIH U54 AA019765 (06-10), P.I., “Mechanisms of Alcohol Pathology: A Collaborative Partnership Between NCCU & UNC”, $4,722,071 total costs.