Nigel G. F. Cooper, Ph.D., Professor and Vice Chair for Research

E-Mail:nigelcooper@louisville.edu
Phone: 502-852-1474

Dr. Cooper’s research is related to plasticity in the nervous system.  His most recent work relates to observations on plasticity in the retina.  For example, he has shown that the quantity and quality of synaptic receptor molecules in the retina are altered in response to environmental stimulation, only in a limited period during development.  Thus, the composition of retinal NMDA-receptors is altered by light deprivation in neonates but not in adult rats.  In a separate but related area of study he has shown that stimulation of NMDA-receptors in the retina can lead to the enhanced transcription of apoptosis-associated genes in amacrine and ganglion cell layers of the retina.  The aim of this second focus area is to develop a model for the study of certain neurodegenerative processes, with the hope of uncovering the signal transduction pathway between the stimulus and cell death.  With this knowledge the most appropriate sites for neurotherapeutic intervention can be targeted so that neurons can be protected during periods of stress.

Representative Publications: Khalyfa A, Chlon T, Qiang H, Agarwak N, Cooper NG. (2007) Microarray reveals complement components are regulated in the serum-deprived rat retinal ganglion cell line. Mol Vis., 13:293-308.

Fan W, Agarwal N, Cooper NG. (2006) The role of CaMKII in BDNF-mediated neuroprotection of retinal ganglion cells (RGC-5). Brain Res., 1067(1):48-57.

Fan W, Agarwal N, Kumar MD, Cooper NG. (2005) Retinal ganglion cell death and neuroprotection: Involvement of the CaMKII alpha gene. Mol Brain Res., 139(2):306-16.

Xue J, Cooper NGF (2001) The modification of NMDA receptors by visual experience in the rat retina is age dependent. Mol Brain Res., 91:196-203.