Peter F Hitchcock Ph.D.
| W. K. Kellogg Eye Center, 0714 |
| Ann Arbor, MI 48109 |
Download this page 
Our laboratory is investigating persistent and injury-induced neurogenesis in the retina of teleost fish. A hallmark of the human central nervous system is that injuries are not repaired.
Neurons lost to stroke or trauma are never replaced. In contrast, injuries to the retina of some teleost fish stimulate stem-cell based neurogenesis in the area of the wound, regeneration of the destroyed neurons and functional recovery.
Our studies indicate that neuronal regeneration in the retina of adult fish utilizes the cellular and molecular mechanisms that are present in the embryonic retina and brain; retinal regeneration recapitulates retinal ontogeny. In contrast to the mammalian retina, the retina of the adult fish remains permissive for events normally confined to the embryo. A variety of approaches are being used to study regenerative neurogenesis, from examining the cellular and synaptic anatomy of the regenerated retina to testing the function of genes that participate in the injury response and the regeneration of new neurons.
Current studies are focused on the cellular expression patterns and function of genes that encode developmental regulatory proteins, growth factors and growth factor receptors.
Raymond, P.A., Hitchcock, P.F. (2000) How the neural retina regenerates. Results & Problems in Cell Differentiation. 31:197-218.
Otteson, D.C., D'Costa, A.R., Hitchcock, P.F. (2001) Putative stem cells and the lineage of rod photoreceptors in the mature retina of the goldfish. Developmental Biology. 232:62-76.
Otteson, D.C., Cirenza, P.F. Hitchcock, P.F. (2002) Persistent neurogenesis in the teleost retina: evidence for regulation by the growth-hormone/insulin-like growth factor-I axis. Mech. Dev. 117:137-149.
Otteson, D.C., Hitchcock, P.F. (2003) Stem cells in the teleost retina: persistent neurogenesis and injury-induced regeneration. Vision Res. 43:927-936.
Hitchcock, P.F., M. Ochocinska, A. Sieh, D. C. Otteson (2004) Persistent and injury-induced neurogenesis in the vertebrate retina. Prog. Retinal Res. 23:183-194.
Hitchcock, P.F. and L. Kakuk-Atkins (2004) The bHLH transcription factor neuroD is expressed in the rod lineage of the teleost retina. J. Comp. Neurol., 477(1):108-17.
Ayayagari, R., M.N.A. Mandal, A. J. Karoukis, L. Chen., N.C. McLaren, M. Lichter, D.T. Wong, P. F. Hitchcock, R.C.. Caruso, S.E. Moroi, I.H. Maumenee, P.A. Sieving. (2005) Late-onset macular degeneration and long anterior lens zonules result from a CTRP5 gene mutation. Invest. Ophthal. Visual Sci., 46:3363-3371.
Chang B, Dacey MS, Hawes NL, Hitchcock PF, Milam AH, Atmaca-Sonmez P, Nusinowitz S, Heckenlively JR. (2006) Cone photoreceptor function loss-3, a novel mouse model of achromatopsia due to a mutation in Gnat2. Invest Ophthalmol Vis Sci.47:5017-21.
Mandal MN, Vasireddy V, Reddy GB, Wang X, Moroi SE, Pattnaik BR, Hughes BA, Heckenlively JR, Hitchcock PF, Jablonski MM, Ayyagari R.(2006) CTRP5 is a membrane-associated and secretory protein in the RPE and ciliary body and the S163R mutation of CTRP5 impairs its secretion. Invest Ophthalmol Vis Sci. 2006 47:5505-13.
Ochocinska, M and P.F. Hitchcock. (2007) Cellular expression of the bHLH transcription factor, neuroD, in the retina of the embryonic and larval zebrafish. J. Comp. Neurol. 501:1-12
Find more publications by Dr.Peter Hitchcock