Science Inventory

CHANGES IN NEUROTRANSMITTER GENE EXPRESSION IN THE AGING RETINA.

Citation:

ROYLAND, J. E. CHANGES IN NEUROTRANSMITTER GENE EXPRESSION IN THE AGING RETINA. Presented at American Society of Neurochemistry, Portland, OR, March 11 - 14, 2006.

Description:

To understand mechanisms of neurotoxicity in susceptible populations, we examined age-related changes in constitutive gene expression in the retinas of young (4mos), middle-aged (11 mos) and aged (23 mos) male Long Evans rats. Derived from a pouch of the forebrain during development, the retina is a good model for studying neurological age-related risk factors. Its complex morphology mimics the synaptic connections and neural networks of the brain. Its position outside the brain allows for easy access for in vivo functional studies. And age has been shown to be a co-factor in retinal degeneration caused by fungicides and organophosphate insecticides. Declining visual ability during normal aging is due in part to changes in the retina or central visual pathways. Generation of the visual signal is a highly coordinated and regulated process with individual cells utilizing specific neurotransmitters to carry out specific functions that shape receptive field properties. Genomic analysis using the Affymetrix rat 230A gene chip revealed a number of genes involved in neural transmission to be significantly changed with aging. Eighteen genes associated with glutamate (neurotransmitters, receptors, channels, etc), the major neurotransmitter from photoreceptors to bipolar cells to ganglion cells, were differentially expressed between 4 and 23 mos of age, with the greatest change occurring between 11 and 23 mos. Changes in dopaminergic, gabergic, and cholinergic genes which serve modulatory roles in the retina were also detected. We report here possible interactions/pathways between these neurotransmitters and how changes found may impact functional capacity. Our goal is to understand how age-related changes in signal transmission/modulation may play a role in susceptibility. This abstract does not necessarily reflect US EPA policy.

Record Details:

Record Type: DOCUMENT (PRESENTATION/ABSTRACT)
Product Published Date: 03/12/2006
Record Last Revised: 06/21/2006
Record ID: 146304

Organization:

U.S. ENVIRONMENTAL PROTECTION AGENCY

OFFICE OF RESEARCH AND DEVELOPMENT

NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LABORATORY

NEUROTOXICOLOGY DIVISION

CELLULAR AND MOLECULAR TOXICOLOGY BRANCH